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Inflammatory myopathy

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Inflammatory myopathy
Other namesIdiopathic inflammatory myopathy
Image
Gottron's papules on the hand of a patient with juvenile dermatomyositis
SpecialtyRheumatology Edit this on Wikidata

Inflammatory myopathy (IM), is a collection of autoimmune systemic diseases characterised by muscle inflammation, and frequently accompanied by extramuscular manifestations affecting the skin, lung, and joints.[1][2] The main classes of inflammatory myopathy are dermatomyositis (DM) (including juvenile, amyopathic, and sine-dermatitis form), the antisynthetase syndrome (ASyS), inclusion-body myositis (IBM), immune-mediated necrotising myopathy (IMNM). Polymyositis (PM) is nowadays a diagnosis of exclusion.[1][2]

Diagnosis

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There are several diagnostic and classification criteria for the different forms of myositis. Most contemporary approaches integrate clinical features with autoantibody testing and other complementary investigations.[3][4][5][6] Some criteria are broad and support a syndromic diagnosis, such as DM or IMNM,[3][4][5] whereas others are more granular and allow identification of autoantibody-defined entities.[6]

In patients with compatible clinical features, several diagnostic tests can help establish the diagnosis and distinguish among the different forms of myositis. Muscle enzymes, such as creatine kinase and aldolase, are released into the circulation when muscle fibers are damaged. They are useful markers of muscle necrosis and are often the first laboratory abnormality suggesting inflammatory myositis.

Myositis-specific and myositis-associated autoantibodies have emerged as key diagnostic markers. In combination with characteristic clinical features, they may be sufficient to diagnose certain forms of inflammatory myositis, even in the absence of confirmatory tests such as muscle biopsy.[4][5][6] Muscle biopsy remains particularly useful when specific autoantibodies are absent, when the clinical picture is atypical, or when alternative diagnoses need to be excluded.

Electromyography can help identify myopathic changes consistent with myositis and exclude neuropathic processes.[7] Muscle MRI is useful for distinguishing active inflammation from chronic damage and for selecting an appropriate biopsy site.[8] Muscle ultrasound can also detect muscle inflammation and, in specialized centers, may be used to support diagnosis, monitor disease progression, and guide biopsy site selection.[9]

Nailfold videocapillaroscopy, which assesses abnormalities of the nailbed capillaries, is useful for detecting microvascular changes in myositis and may also help monitor treatment response.[10][11] Dynamometry provides a more objective assessment of muscle strength and can be useful for evaluating disease severity and tracking changes over time.

Epidemiology

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Every year between 2.18 and 7.7 people per million receive a diagnosis of PM or DM.[12] Around 3.2 children per million per year are diagnosed with DM (termed juvenile dermatomyositis), with an average age of onset of seven years. Diagnosis of adult DM commonly occurs between 30 and 50 years of age. PM is an adult disease, usually emerging after the age of twenty. PM and DM are more common in females, more common in Caucasians, and least common in Asians. At any given time, about 35.5 people per million have IBM; it emerges after the age of 30 (usually after 50), and may be more common in males.[13]

Etiology

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The etiology of myositis is thought to involve an interaction between genetic susceptibility, environmental exposures, infections, medications, malignancy, and autoimmune responses. Different subtypes are associated with distinct clinical, histological, molecular, and autoantibody profiles.[1][2]

Several triggers have been implicated. Ultraviolet radiation has been associated with dermatomyositis, while dust and air pollutants have been linked to inflammatory myopathy risk.[14][15][16][17] Viral infections may contribute to some forms of disease, particularly anti-MDA5 dermatomyositis with interstitial lung disease, which shows seasonal clustering.[18][19] Cancer is strongly associated with some forms of dermatomyositis, especially anti-TIF1γ-positive disease, in which tumor mutations may initiate an immune response that later cross-reacts with regenerating muscle and skin.[20][21][22] Drug exposures can also trigger myositis; statins are associated with anti-HMGCR immune-mediated necrotizing myopathy,[23] and immune checkpoint inhibitors can induce several transcriptomically and histologically distinct forms of myositis.[24] Finally, bone marrow transplant can induce IM.[25]

Genetic predisposition is also important, particularly variation in human leukocyte antigen genes. Specific HLA alleles are associated with autoantibody-defined subgroups.[26][27][28]

Pathogenesis

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Recent studies suggest that the pathogenesis of several non-IBM forms of IM are driven by the pathogenic internalization of autoantibodies.[29][30][31] Although these antibodies target intracellular proteins, evidence indicates that they can enter different cell types and disrupt the function of their target autoantigens causing inflammation and damage.[30][31] For example, anti-Mi-2 autoantibodies bind PHD-containing proteins,[32][33] including component of the NuRD complex, inducing derepression of multiple genes;[30] anti-PM/Scl antibodies impair the nuclear RNA exosome complex, leading to accumulation of long non-coding RNAs and divergent transcripts;[30][31] anti-HMGCR autoantibodies disrupt the enzymatic function of HMGCR, inducing accumulation of neutral lipids;[30][34] and anti-Jo-1 antibodies interfere with histidyl-tRNA synthetase function.[30] In anti-MDA5 dermatomyositis, autoantibodies activate MDA5 and contribute to activation of type I interferon pathways.[30]

The type I interferon pathway is especially prominent in dermatomyositis and has become a major therapeutic target.[35][36] Clinical responses to JAK inhibitors,[37][38][39][40][41] anti-IFNβ therapy,[42] and agents targeting the interferon receptor support the importance of this pathway in disease activity. Conversely, a negative trial of complement inhibition in immune-mediated necrotizing myopathy[43] has challenged earlier models in which complement-mediated muscle injury was considered central to that subtype.[44][45][46]

Inclusion body myositis remains the least well-understood form of myositis. Its pathogenesis is thought to involve both inflammatory and degenerative mechanisms, including cytotoxic T-cell infiltration,[47] which in many cases fulfills criteria for large granular lymphocytic leukemia,[48] as well as TDP-43 dysfunction characterized by nuclear depletion, cytoplasmic mislocalization, and the appearance of cryptic exons.[49] Anti-NT5C1A autoantibodies are detected in some patients,[50] but they are not specific for inclusion body myositis,[51] and their pathogenic significance remains uncertain. Overall, no single unifying pathogenic mechanism has been established.

Treatment

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Multiple effective therapies are available for the treatment of non-IBM forms of IM.[1] Standard treatment typically consists of a combination of glucocorticoids and steroid-sparing immunosuppressive agents, including methotrexate, mycophenolate mofetil, azathioprine, tacrolimus, and cyclosporine. Intravenous immunoglobulin (IVIG) has demonstrated efficacy in DM and is widely used to control disease activity across several IM subtypes.[52][53] Although rituximab did not meet its primary endpoint in randomized clinical trials, it remains an important treatment option in clinical practice, particularly for refractory disease, often in combination with IVIG.[54]

More recently, Janus kinase (JAK) inhibitors, including tofacitinib,[55] ruxolitinib,[56][57] baricitinib,[58] and brepocitinib,[59] have shown efficacy in dermatomyositis. Additional strategies targeting the type I interferon pathway have also demonstrated benefit, including blockade of interferon-β with dazukibart.[60]

Deep B-cell depletion with CD19 chimeric antigen receptor (CAR) T-cell therapy has shown preliminary evidence of inducing sustained, and potentially treatment-free, remission in IM.[61] Similarly, plasma cell–targeted therapies, including CAR T-cell approaches[62] and monoclonal antibodies,[63] as well as inhibitors of the neonatal Fc receptor (FcRn), such as efgartigimod,[64] have emerged as promising therapeutic strategies for IM.

Overall, with timely diagnosis and appropriate treatment, the prognosis of DM, ASyS, IMNM, and other non-IBM inflammatory myopathies is generally favorable.

Inclusion-body myositis

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Despite its clinical similarities to other forms of IM, IBM does not respond to therapies that are effective in other IM subtypes, and no treatment has yet been proven to alter its disease course. Numerous therapeutic agents have been evaluated in clinical trials, including methotrexate,[65] IVIG,[66] alemtuzumab,[67] bimagrumab,[68] sirolimus,[69] arimoclomol,[70] and ulviprubart[71] but none has demonstrated definitive clinical efficacy.[72] Non-fatiguing, systematic strength-building exercise has demonstrated benefit.[73] Occupational and rehabilitation therapists can offer good advice on walking without falling and performing fine motor tasks, and can provide appropriate canes, braces and wheelchairs. Speech pathologists can provide advice on preventing choking episodes and reducing the anxiety of an immanent aspiration for both patients and carers.[74]

Differential diagnoses

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IM should be distinguished from a broad range of conditions that can present with similar clinical features, including infections, muscle trauma, medications and toxins, inherited and metabolic myopathies, neuromuscular junction disorders (such as Lambert–Eaton myasthenic syndrome and myasthenia gravis), and systemic autoimmune diseases, including systemic sclerosis, systemic lupus erythematosus and sarcoidosis.[75][76]

See also

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References

[edit]
  1. 1 2 3 4 Selva-O'Callaghan, Albert; Pinal-Fernandez, Iago; Trallero-Araguás, Ernesto; Milisenda, José César; Grau-Junyent, Josep Maria; Mammen, Andrew L. (2018-09-01). "Classification and management of adult inflammatory myopathies". The Lancet. Neurology. 17 (9): 816–828. doi:10.1016/S1474-4422(18)30254-0. ISSN 1474-4465. PMC 11646336. PMID 30129477.
  2. 1 2 3 Allenbach, Yves; Benveniste, Olivier (2026-05-14). "Inflammatory Myopathies". The New England Journal of Medicine. 394 (19): 1925–1938. doi:10.1056/NEJMra2415426. ISSN 1533-4406. PMID 42127392.
  3. 1 2 Lundberg, Ingrid E.; Tjärnlund, Anna; Bottai, Matteo; Werth, Victoria P.; Pilkington, Clarissa; Visser, Marianne de; Alfredsson, Lars; Amato, Anthony A.; Barohn, Richard J.; Liang, Matthew H.; Singh, Jasvinder A.; Aggarwal, Rohit; Arnardottir, Snjolaug; Chinoy, Hector; Cooper, Robert G. (2017-12-01). "2017 European League Against Rheumatism/American College of Rheumatology classification criteria for adult and juvenile idiopathic inflammatory myopathies and their major subgroups". Annals of the Rheumatic Diseases. 76 (12): 1955–1964. doi:10.1136/annrheumdis-2017-211468. ISSN 1468-2060. PMC 5736307. PMID 29079590.
  4. 1 2 3 Allenbach, Yves; Mammen, Andrew L.; Benveniste, Olivier; Stenzel, Werner; Immune-Mediated Necrotizing Myopathies Working Group (2018-01-01). "224th ENMC International Workshop:: Clinico-sero-pathological classification of immune-mediated necrotizing myopathies Zandvoort, The Netherlands, 14-16 October 2016". Neuromuscular Disorders: NMD. 28 (1): 87–99. doi:10.1016/j.nmd.2017.09.016. ISSN 1873-2364. PMID 29221629.
  5. 1 2 3 Mammen, Andrew L.; Allenbach, Yves; Stenzel, Werner; Benveniste, Olivier; ENMC 239th Workshop Study Group (2020-01-01). "239th ENMC International Workshop: Classification of dermatomyositis, Amsterdam, the Netherlands, 14-16 December 2018". Neuromuscular Disorders: NMD. 30 (1): 70–92. doi:10.1016/j.nmd.2019.10.005. ISSN 1873-2364. PMID 31791867.{{cite journal}}: CS1 maint: numeric names: authors list (link)
  6. 1 2 3 Casal-Dominguez, Maria; Pinal-Fernandez, Iago; Pak, Katherine; Huang, Wilson; Selva-O'Callaghan, Albert; Albayda, Jemima; Casciola-Rosen, Livia; Paik, Julie J.; Tiniakou, Eleni; Mecoli, Christopher A.; Lloyd, Thomas E.; Danoff, Sonye K.; Christopher-Stine, Lisa; Mammen, Andrew L. (2022-03-01). "Performance of the 2017 European Alliance of Associations for Rheumatology/American College of Rheumatology Classification Criteria for Idiopathic Inflammatory Myopathies in Patients With Myositis-Specific Autoantibodies". Arthritis & Rheumatology (Hoboken, N.J.). 74 (3): 508–517. doi:10.1002/art.41964. ISSN 2326-5205. PMC 8881307. PMID 34480833.
  7. ↑ Paganoni, Sabrina; Amato, Anthony (2013-02-01). "Electrodiagnostic evaluation of myopathies". Physical Medicine and Rehabilitation Clinics of North America. 24 (1): 193–207. doi:10.1016/j.pmr.2012.08.017. ISSN 1558-1381. PMC 4435557. PMID 23177039.
  8. ↑ Pinal-Fernandez, Iago; Casal-Dominguez, Maria; Carrino, John A.; Lahouti, Arash H.; Basharat, Pari; Albayda, Jemima; Paik, Julie J.; Ahlawat, Shivani; Danoff, Sonye K.; Lloyd, Thomas E.; Mammen, Andrew L.; Christopher-Stine, Lisa (2017-04-01). "Thigh muscle MRI in immune-mediated necrotising myopathy: extensive oedema, early muscle damage and role of anti-SRP autoantibodies as a marker of severity". Annals of the Rheumatic Diseases. 76 (4): 681–687. doi:10.1136/annrheumdis-2016-210198. ISSN 1468-2060. PMC 6019551. PMID 27651398.
  9. ↑ Albayda, Jemima; van Alfen, Nens (2020-09-28). "Diagnostic Value of Muscle Ultrasound for Myopathies and Myositis". Current Rheumatology Reports. 22 (11): 82. doi:10.1007/s11926-020-00947-y. ISSN 1534-6307. PMC 7522112. PMID 32989482.
  10. ↑ Torres-Ruiz, Jiram; Pinal-Fernandez, Iago; Selva-O'Callaghan, Albert; Campbell, Bianca; Muñoz-Braceras, Sandra; Mejía-Domínguez, Nancy R.; Núñez-Álvarez, Carlos; Milisenda, José; Casal-Domínguez, Maria; Pak, Katherine; Guillén-del-Castillo, Alfredo; Trallero-Araguas, Ernesto; Gil-Vila, Albert; Mammen, Andrew Lee (2024-03-14). "Nailfold capillaroscopy findings of a multicentric multi-ethnic cohort of patients with idiopathic inflammatory myopathies". Clinical and Experimental Rheumatology. 42 (2): 367–376. doi:10.55563/clinexprheumatol/l9gudh. ISSN 1593-098X. PMC 11669110. PMID 38488092.
  11. ↑ Pinal-Fernandez, I.; Fonollosa-Pla, V.; Selva-O'Callaghan, A. (2016-03-01). "Improvement of the nailfold capillaroscopy after immunosuppressive treatment in polymyositis". QJM: Monthly Journal of the Association of Physicians. 109 (3): 205–206. doi:10.1093/qjmed/hcv196. ISSN 1460-2393. PMC 4830223. PMID 26454514.
  12. ↑ Mastaglia FL, Garlepp MJ, Phillips BA, Zilko PJ (April 2003). "Inflammatory myopathies: clinical, diagnostic and therapeutic aspects". Muscle & Nerve. 27 (4): 407–425. doi:10.1002/mus.10313. PMID 12661042. S2CID 24978554. Cited in:
    • Holton JL, Wedderburn LR, Hanna MG (29 May 2013). "Polymyositis, Dermatomyositis and Inclusion Body Myositis". In Goebel HH, Sewry CA, Weller RO (eds.). Muscle Disease: Pathology and Genetics. John Wiley & Sons. pp. 747–781. ISBN 978-1-118-63549-0.
  13. ↑ Holton JL, Wedderburn LR, Hanna MG (29 May 2013). "Polymyositis, Dermatomyositis and Inclusion Body Myositis". In Goebel HH, Sewry CA, Weller RO (eds.). Muscle Disease: Pathology and Genetics. John Wiley & Sons. pp. 747–781. ISBN 978-1-118-63549-0.
  14. ↑ Love, Lori A.; Weinberg, Clarice R.; McConnaughey, D. Robert; Oddis, Chester V.; Medsger, Thomas A.; Reveille, John D.; Arnett, Frank C.; Targoff, Ira N.; Miller, Frederick W. (2009-07-30). "Ultraviolet radiation intensity predicts the relative distribution of dermatomyositis and anti–Mi-2 autoantibodies in women". Arthritis & Rheumatism. 60 (8): 2499–2504. doi:10.1002/art.24702. ISSN 0004-3591. PMC 2855681. PMID 19644877.
  15. ↑ Orione, Maria Angélica M.; Silva, Clovis A.; Sallum, Adriana M. E.; Campos, Lúcia M. A.; Omori, Clarissa H.; Braga, Alfésio L. F.; Farhat, Sylvia C. L. (2014-09-25). "Risk Factors for Juvenile Dermatomyositis: Exposure to Tobacco and Air Pollutants During Pregnancy". Arthritis Care & Research. 66 (10): 1571–1575. doi:10.1002/acr.22358. ISSN 2151-464X. PMID 24757124.
  16. ↑ Labirua-Iturburu, Ane; Selva-O'Callaghan, Albert; Zock, Jan-Paul; Orriols, Ramon; Martínez-Gómez, Xavier; Vilardell-Tarrés, Miquel (2014-01-03). "Occupational exposure in patients with the antisynthetase syndrome". Clinical Rheumatology. 33 (2): 221–225. doi:10.1007/s10067-013-2467-0. ISSN 0770-3198. PMID 24384826.
  17. ↑ Miller-Archie, Sara A.; Izmirly, Peter M.; Berman, Jessica R.; Brite, Jennifer; Walker, Deborah J.; Dasilva, Renato C.; Petrsoric, Lysa J.; Cone, James E. (2020-04-01). "Systemic Autoimmune Disease Among Adults Exposed to the September 11, 2001 Terrorist Attack". Arthritis & Rheumatology. 72 (5): 849–859. doi:10.1002/art.41175. ISSN 2326-5191. PMC 7216890. PMID 31762219.
  18. ↑ Nishina, Naoshi; Sato, Shinji; Masui, Kenichi; Gono, Takahisa; Kuwana, Masataka (2020-06-01). "Seasonal and residential clustering at disease onset of anti-MDA5-associated interstitial lung disease". RMD Open. 6 (2) e001202. doi:10.1136/rmdopen-2020-001202. ISSN 2056-5933. PMC 7299503. PMID 32506053.
  19. ↑ Toquet, Ségolène; Granger, Benjamin; Uzunhan, Yurdagul; Mariampillai, Kubéraka; Nunes, Hilario; Benveniste, Olivier; Allenbach, Yves (2021-04-01). "The seasonality of Dermatomyositis associated with anti-MDA5 antibody: An argument for a respiratory viral trigger". Autoimmunity Reviews. 20 (4) 102788. doi:10.1016/j.autrev.2021.102788. ISSN 1568-9972. PMID 33609802.
  20. ↑ Pinal-Fernandez, Iago; Ferrer-Fabregas, Berta; Trallero-Araguas, Ernesto; Balada, Eva; Martínez, Maria Angeles; Milisenda, Jose César; Aparicio-Español, Gloria; Labrador-Horrillo, Moises; Garcia-Patos, Vicente; Grau-Junyent, Josep M; Selva-O'Callaghan, Albert (2017-11-14). "Tumour TIF1 mutations and loss of heterozygosity related to cancer-associated myositis". Rheumatology. 57 (2): 388–396. doi:10.1093/rheumatology/kex413. ISSN 1462-0324. PMC 5850766. PMID 29149307.
  21. ↑ Cordel, Nadège; Derambure, Céline; Coutant, Sophie; Mariette, Xavier; Jullien, Denis; Debarbieux, Sébastien; Chosidow, Olivier; Meyer, Alain; Bessis, Didier; Joly, Pascal; Mathian, Alexis; Levesque, Hervé; Sabourin, Jean-Christophe; Tournier, Isabelle; Boyer, Olivier (2021-03-25). "TRIM33 gene somatic mutations identified by next generation sequencing in neoplasms of patients with anti-TIF1γ positive cancer-associated dermatomyositis". Rheumatology. 60 (12): 5863–5867. doi:10.1093/rheumatology/keab260. ISSN 1462-0324. PMID 33764396.
  22. ↑ Moreno-Cárdenas, Ana Belén; Ros, Javier; Gil-Vila, Albert; Datta, Debayan; Fasani, Roberta; Serna, Garazi; Jimenez, Jose; Trallero-Araguás, Ernesto; Viaplana, Cristina; Lostes, Julia; Milisenda, José César; Grau-Junyent, Josep Maria; Lopez-Perez, Raquel; Pinal-Fernández, Iago; Nuciforo, Paolo (2026-03-01). "Frequent genetic alterations in myositis autoantigen genes in cancer-associated dermatomyositis". Annals of the Rheumatic Diseases. 85 (3): 519–533. doi:10.1016/j.ard.2025.10.018. ISSN 0003-4967. PMC 13137219. PMID 41290487.
  23. ↑ Mammen, Andrew L. (2016-02-18). Longo, Dan L. (ed.). "Statin-Associated Autoimmune Myopathy". New England Journal of Medicine. 374 (7): 664–669. doi:10.1056/NEJMra1515161. ISSN 0028-4793. PMID 26886523.
  24. ↑ Pinal-Fernandez, Iago; Quintana, Angela; Milisenda, Jose Cesar; Casal-Dominguez, Maria; Muñoz-Braceras, Sandra; Derfoul, Assia; Torres-Ruiz, Jiram; Pak, Katherine; Dell'Orso, Stefania; Naz, Faiza; Gutierrez-Cruz, Gustavo; Milone, Margherita; Shelly, Shahar; Duque-Jaimez, Yaiza; Tobias-Baraja, Ester (2023-06-01). "Transcriptomic profiling reveals distinct subsets of immune checkpoint inhibitor induced myositis". Annals of the Rheumatic Diseases. 82 (6): 829–836. doi:10.1136/ard-2022-223792. ISSN 1468-2060. PMC 10545139. PMID 36801811.
  25. ↑ Saw, Jacqui-Lyn; Sidiqi, M. Hasib; Mauermann, Michelle L.; Alkhateeb, Hassan; Naddaf, Elie (2021-06-01). "Immune-mediated neuromuscular complications of graft-versus-host disease". Muscle & Nerve. 63 (6): 852–860. doi:10.1002/mus.27214. ISSN 1097-4598. PMID 33651380.
  26. ↑ Miller, F W; Chen, W; O'Hanlon, T P; Cooper, R G; Vencovsky, J; Rider, L G; Danko, K; Wedderburn, L R; Lundberg, I E; Pachman, L M; Reed, A M; Ytterberg, S R; Padyukov, L; Selva-O'Callaghan, A; Radstake, T R (2015-08-20). "Genome-wide association study identifies HLA 8.1 ancestral haplotype alleles as major genetic risk factors for myositis phenotypes". Genes & Immunity. 16 (7): 470–480. doi:10.1038/gene.2015.28. ISSN 1466-4879. PMC 4840953. PMID 26291516.
  27. ↑ Mammen, Andrew L.; Gaudet, Daniel; Brisson, Diane; Christopher-Stine, Lisa; Lloyd, Thomas E.; Leffell, Mary S.; Zachary, Andrea A. (2012-07-27). "Increased frequency of DRB1*11:01 in anti–hydroxymethylglutaryl-coenzyme A reductase–associated autoimmune myopathy". Arthritis Care & Research. 64 (8): 1233–1237. doi:10.1002/acr.21671. ISSN 2151-464X. PMC 3400716. PMID 22422616.
  28. ↑ Rothwell, Simon; Chinoy, Hector; Lamb, Janine A; Miller, Frederick W; Rider, Lisa G; Wedderburn, Lucy R; McHugh, Neil J; Mammen, Andrew L; Betteridge, Zoe E; Tansley, Sarah L; Bowes, John; Vencovský, Jiří; Deakin, Claire T; Dankó, Katalin; Vidya, Limaye (2019-07-01). "Focused HLA analysis in Caucasians with myositis identifies significant associations with autoantibody subgroups". Annals of the Rheumatic Diseases. 78 (7): 996–1002. doi:10.1136/annrheumdis-2019-215046. ISSN 0003-4967. PMC 6585280. PMID 31138531.
  29. ↑ Pinal-Fernandez, Iago; Milisenda, Jose Cesar; Pak, Katherine; Muñoz-Braceras, Sandra; Casal-Dominguez, Maria; Torres-Ruiz, Jiram; Dell'Orso, Stefania; Naz, Faiza; Gutierrez-Cruz, Gustavo; Duque-Jaimez, Yaiza; Matas-Garcia, Ana; Padrosa, Joan; Garcia-Garcia, Francesc J.; Guitart-Mampel, Mariona; Garrabou, Gloria (2023-08-01). "Transcriptional derepression of CHD4/NuRD-regulated genes in the muscle of patients with dermatomyositis and anti-Mi2 autoantibodies". Annals of the Rheumatic Diseases. 82 (8): 1091–1097. doi:10.1136/ard-2023-223873. ISSN 1468-2060. PMC 11611052. PMID 37130727.
  30. 1 2 3 4 5 6 7 Pinal-Fernandez, Iago; Muñoz-Braceras, Sandra; Casal-Dominguez, Maria; Pak, Katherine; Torres-Ruiz, Jiram; Musai, Jon; Dell'Orso, Stefania; Naz, Faiza; Islam, Shamima; Gutierrez-Cruz, Gustavo; Cano, Maria Dolores; Matas-Garcia, Ana; Padrosa, Joan; Tobias-Baraja, Ester; Garrabou, Gloria (2024-10-21). "Pathological autoantibody internalisation in myositis". Annals of the Rheumatic Diseases. 83 (11): 1549–1560. doi:10.1136/ard-2024-225773. ISSN 1468-2060. PMC 11493519. PMID 38902010.
  31. 1 2 3 Pinal-Fernandez, Iago; Pak, Katherine; Casal-Dominguez, Maria; Muñoz-Braceras, Sandra; Wigerblad, Gustaf; Dell'Orso, Stefania; Naz, Faiza; Islam, Shamima; Gutierrez-Cruz, Gustavo; Kinder, Travis B.; Ogbonnaya-Whittlesey, S. Amara; Fernández-Codina, Andreu; Giannini, Margherita; Ellezam, Benjamin; Laverny, Gilles (2026-03-05). "Spatial transcriptomics reveals mechanism of autoimmunity driven by internalized autoantibodies". medRxiv 10.64898/2026.02.14.26346329.
  32. ↑ Musai, Jon; Jayaraman, Sahana; Pak, Katherine; Pinal-Fernandez, Iago; Muñoz-Braceras, Sandra; Casal-Dominguez, Maria; Cho, Eric; Fitisemanu, Fa'alataitaua M.; Burbelo, Peter D.; Kaplan, Mariana J.; Warner, Blake M.; Schiffenbauer, Adam I.; Selva-O'Callaghan, Albert; Milisenda, José César; Rider, Lisa G. (2026-02-01). "Myositis-specific autoantibodies recognising Mi2 also target the AIRE protein at a shared PHD zinc finger". Annals of the Rheumatic Diseases. 85 (2): 351–359. doi:10.1016/j.ard.2025.08.023. ISSN 1468-2060. PMC 12676962. PMID 40957771.
  33. ↑ Pinal-Fernandez, Iago; Musai, Jon; Casal-Dominguez, Maria; Pak, Katherine; Kaplan, Mariana; Warner, Blake M.; Rider, Lisa G.; Aggarwal, Rohit; Oddis, Chester V.; Moghadam-Kia, Siamak; Garrabou, Gloria; Selva-O'Callaghan, Albert; Milisenda, Jose C.; Chiorini, John A.; Mammen, Andrew L. (2025-12-01). "Anti-Mi2 autoantibodies target PHD fingers of SP140L and TIF1γ, while anti-TIF1γ autoantibodies primarily bind TIF1γ outside the PHD region". Rheumatology (Oxford, England). 64 (12): 6371–6377. doi:10.1093/rheumatology/keaf426. ISSN 1462-0332. PMC 12671865. PMID 40795062.
  34. ↑ Giannini, Margherita; Quiring, Giulia; Oulad-Abdelghani, Mustapha; Lannes, Béatrice; Allenbach, Yves; Benveniste, Olivier; Boyer, Olivier; Pakleza, Aleksandra Nadaj; Geny, Bernard; Meyer, Alain (2025-10-01). "In immune-mediated necrotising myopathy, anti-HMGCR antibodies inhibit HMGCR activity, leading to the sarcoplasmic accumulation of lipid droplets and myofibres necrosis". Annals of the Rheumatic Diseases. 84 (10): 1752–1755. doi:10.1016/j.ard.2025.04.027. ISSN 1468-2060. PMID 40410054.
  35. ↑ Greenberg, Steven A.; Pinkus, Jack L.; Pinkus, Geraldine S.; Burleson, Travis; Sanoudou, Despina; Tawil, Rabi; Barohn, Richard J.; Saperstein, David S.; Briemberg, Hannah R.; Ericsson, Maria; Park, Peter; Amato, Anthony A. (2005-05-01). "Interferon-alpha/beta-mediated innate immune mechanisms in dermatomyositis". Annals of Neurology. 57 (5): 664–678. doi:10.1002/ana.20464. ISSN 0364-5134. PMID 15852401.
  36. ↑ Pinal-Fernandez, Iago; Casal-Dominguez, Maria; Derfoul, Assia; Pak, Katherine; Plotz, Paul; Miller, Frederick W.; Milisenda, Jose C.; Grau-Junyent, Josep M.; Selva-O'Callaghan, Albert; Paik, Julie; Albayda, Jemima; Christopher-Stine, Lisa; Lloyd, Thomas E.; Corse, Andrea M.; Mammen, Andrew L. (2019-09-17). "Identification of distinctive interferon gene signatures in different types of myositis". Neurology. 93 (12): e1193–e1204. doi:10.1212/WNL.0000000000008128. ISSN 1526-632X. PMC 6808530. PMID 31434690.
  37. ↑ Hornung, Thorsten; Janzen, Viktor; Heidgen, Franz-Josef; Wolf, Dominik; Bieber, Thomas; Wenzel, Joerg (2014-12-25). "Remission of Recalcitrant Dermatomyositis Treated with Ruxolitinib". New England Journal of Medicine. 371 (26): 2537–2538. doi:10.1056/nejmc1412997. ISSN 0028-4793. PMID 25539124.
  38. ↑ Ladislau, Leandro; Suárez-Calvet, Xavier; Toquet, Ségolène; Landon-Cardinal, Océane; Amelin, Damien; Depp, Marine; Rodero, Mathieu P; Hathazi, Denisa; Duffy, Darragh; Bondet, Vincent; Preusse, Corinna; Bienvenu, Boris; Rozenberg, Flore; Roos, Andreas; Benjamim, Claudia F (2018-05-08). "JAK inhibitor improves type I interferon induced damage: proof of concept in dermatomyositis". Brain. 141 (6): 1609–1621. doi:10.1093/brain/awy105. ISSN 0006-8950. PMID 29741608.
  39. ↑ Paik, Julie J.; Casciola-Rosen, Livia; Shin, Joseph Yusup; Albayda, Jemima; Tiniakou, Eleni; Leung, Doris G.; Gutierrez-Alamillo, Laura; Perin, Jamie; Florea, Liliana; Antonescu, Corina; Leung, Sherry G.; Purwin, Grazyna; Koenig, Andrew; Christopher-Stine, Lisa (2021-03-24). "Study of Tofacitinib in Refractory Dermatomyositis: An Open-Label Pilot Study of Ten Patients". Arthritis & Rheumatology. 73 (5): 858–865. doi:10.1002/art.41602. ISSN 2326-5191. PMC 8084900. PMID 33258553.
  40. ↑ Kim, Hanna; Dill, Samantha; O'Brien, Michelle; Vian, Laura; Li, Xiaobai; Manukyan, Manuk; Jain, Minal; Adeojo, Lilian W.; George, Jomy; Perez, Maria; Grom, Alexei A.; Sutter, Michelle; Feldman, Brian M.; Yao, Lawrence; Millwood, Michelle (2021-03-01). "Janus kinase (JAK) inhibition with baricitinib in refractory juvenile dermatomyositis". Annals of the Rheumatic Diseases. 80 (3): 406–408. doi:10.1136/annrheumdis-2020-218690. ISSN 1468-2060. PMC 7904969. PMID 32843325.
  41. ↑ Vleugels, Ruth Ann; Paik, Julie J.; Bauer Ventura, Iazsmin; Mangold, Aaron R.; Gandiga, Prateek C.; Haemel, Anna; Chinoy, Hector; Hussain, Yessar M.; Sivakumar, Kumaraswamy; Griger, Zoltan; Lee, Eun Bong; Bozan, Francisca; Hsu, Chung-Yuan; Femia, Alisa; Dimachkie, Mazen M. (2026-05-14). "A Phase 3 Trial of Brepocitinib in Dermatomyositis". New England Journal of Medicine. 394 (19): 1883–1893. doi:10.1056/NEJMoa2503531. ISSN 0028-4793. PMID 41910335.
  42. ↑ Fiorentino, David; Mangold, Aaron R; Werth, Victoria P; Christopher-Stine, Lisa; Femia, Alisa; Chu, Myron; Musiek, Amy C M; Sluzevich, Jason C; Graham, Lauren V; Fernandez, Anthony P; Aggarwal, Rohit; Rieger, Kerri; Page, Karen M; Li, Xingpeng; Hyde, Craig (2025-01-01). "Efficacy, safety, and target engagement of dazukibart, an IFNβ specific monoclonal antibody, in adults with dermatomyositis: a multicentre, double-blind, randomised, placebo-controlled, phase 2 trial". The Lancet. 405 (10473): 137–146. doi:10.1016/s0140-6736(24)02071-3. ISSN 0140-6736. PMID 39798982.
  43. ↑ Mammen, Andrew L.; Amato, Anthony A.; Dimachkie, Mazen M.; Chinoy, Hector; Hussain, Yessar; Lilleker, James B.; Pinal-Fernandez, Iago; Allenbach, Yves; Boroojerdi, Babak; Vanderkelen, Mark; Delicha, Eumorphia Maria; Koendgen, Harold; Farzaneh-Far, Ramin; Duda, Petra W.; Sayegh, Camil (2023-02-01). "Zilucoplan in immune-mediated necrotising myopathy: a phase 2, randomised, double-blind, placebo-controlled, multicentre trial". The Lancet. Rheumatology. 5 (2): e67–e76. doi:10.1016/s2665-9913(23)00003-6. ISSN 2665-9913. PMC 10009502. PMID 36923454.
  44. ↑ Bergua, Cécile; Chiavelli, Hélène; Allenbach, Yves; Arouche-Delaperche, Louiza; Arnoult, Christophe; Bourdenet, Gwladys; Jean, Laetitia; Zoubairi, Rachid; Guerout, Nicolas; Mahler, Michael; Benveniste, Olivier; Drouot, Laurent; Boyer, Olivier (2019-01-01). "In vivo pathogenicity of IgG from patients with anti-SRP or anti-HMGCR autoantibodies in immune-mediated necrotising myopathy". Annals of the Rheumatic Diseases. 78 (1): 131–139. doi:10.1136/annrheumdis-2018-213518. ISSN 0003-4967. PMID 30309969.
  45. ↑ Allenbach, Yves; Arouche-Delaperche, Louiza; Preusse, Corinna; Radbruch, Helena; Butler-Browne, Gillian; Champtiaux, Nicolas; Mariampillai, Kuberaka; Rigolet, Aude; Hufnagl, Peter; Zerbe, Norman; Amelin, Damien; Maisonobe, Thierry; Louis-Leonard, Sarah; Duyckaerts, Charles; Eymard, Bruno (2018-02-06). "Necrosis in anti-SRP + and anti-HMGCR + myopathies". Neurology. 90 (6): e507–e517. doi:10.1212/wnl.0000000000004923. ISSN 0028-3878. PMID 29330311.
  46. ↑ Julien, Sarah; Vadysirisack, Douangsone; Sayegh, Camil; Ragunathan, Sharan; Tang, Yalan; Briand, Emma; Carrette, Marion; Jean, Laetitia; Zoubairi, Rachid; Gondé, Henri; Benveniste, Olivier; Allenbach, Yves; Drouot, Laurent; Boyer, Olivier (2022-08-20). "Prevention of Anti-HMGCR Immune-Mediated Necrotising Myopathy by C5 Complement Inhibition in a Humanised Mouse Model". Biomedicines. 10 (8): 2036. doi:10.3390/biomedicines10082036. ISSN 2227-9059. PMC 9405589. PMID 36009583.
  47. ↑ Greenberg, Steven A. (2019-05-01). "Inclusion body myositis: clinical features and pathogenesis". Nature Reviews. Rheumatology. 15 (5): 257–272. doi:10.1038/s41584-019-0186-x. ISSN 1759-4804. PMID 30837708.
  48. ↑ Greenberg, Steven A.; Pinkus, Jack L.; Amato, Anthony A.; Kristensen, Thomas; Dorfman, David M. (2016-05-01). "Association of inclusion body myositis with T cell large granular lymphocytic leukaemia". Brain. 139 (5): 1348–1360. doi:10.1093/brain/aww024. ISSN 0006-8950. PMID 26920676.
  49. ↑ Ikenaga, Chiseko; Wilson, Andrew B.; Irwin, Katherine E.; Peethambaran Mallika, Aswathy; Kilgore, Collin; Sinha, Irika R.; Michelle, Elizabeth H.; Ling, Jonathan P.; Wong, Philip C.; Lloyd, Thomas E. (2025-04-01). "Loss of TDP-43 Splicing Repression Occurs in Myonuclei of Inclusion Body Myositis Patients". Annals of Neurology. 97 (4): 629–641. doi:10.1002/ana.27167. ISSN 1531-8249. PMC 13186586. PMID 39757935.
  50. ↑ Larman, H. Benjamin; Salajegheh, Mohammad; Nazareno, Remedios; Lam, Theresa; Sauld, John; Steen, Hanno; Kong, Sek Won; Pinkus, Jack L.; Amato, Anthony A.; Elledge, Stephen J.; Greenberg, Steven A. (2013-03-01). "Cytosolic 5'-nucleotidase 1A autoimmunity in sporadic inclusion body myositis". Annals of Neurology. 73 (3): 408–418. doi:10.1002/ana.23840. ISSN 1531-8249. PMID 23596012.
  51. ↑ Lloyd, Thomas E.; Christopher-Stine, Lisa; Pinal-Fernandez, Iago; Tiniakou, Eleni; Petri, Michelle; Baer, Alan; Danoff, Sonye K.; Pak, Katherine; Casciola-Rosen, Livia A.; Mammen, Andrew L. (2016-01-01). "Cytosolic 5'-Nucleotidase 1A As a Target of Circulating Autoantibodies in Autoimmune Diseases". Arthritis Care & Research. 68 (1): 66–71. doi:10.1002/acr.22600. ISSN 2151-4658. PMC 4887848. PMID 25892010.
  52. ↑ Dalakas, Marinos C.; Illa, Isabel; Dambrosia, James M.; Soueidan, Shawke A.; Stein, Daniel P.; Otero, Carlos; Dinsmore, Steven T.; McCrosky, Susan (1993-12-30). "A Controlled Trial of High-Dose Intravenous Immune Globulin Infusions as Treatment for Dermatomyositis". New England Journal of Medicine. 329 (27): 1993–2000. doi:10.1056/nejm199312303292704. ISSN 0028-4793. PMID 8247075.
  53. ↑ Aggarwal, Rohit; Charles-Schoeman, Christina; Schessl, Joachim; Bata-Csörgő, Zsuzsanna; Dimachkie, Mazen M.; Griger, Zoltan; Moiseev, Sergey; Oddis, Chester; Schiopu, Elena; Vencovský, Jiri; Beckmann, Irene; Clodi, Elisabeth; Bugrova, Olga; Dankó, Katalin; Ernste, Floranne (2022-10-06). "Trial of Intravenous Immune Globulin in Dermatomyositis". The New England Journal of Medicine. 387 (14): 1264–1278. doi:10.1056/NEJMoa2117912. ISSN 1533-4406. PMID 36198179.
  54. ↑ Oddis, Chester V.; Reed, Ann M.; Aggarwal, Rohit; Rider, Lisa G.; Ascherman, Dana P.; Levesque, Marc C.; Barohn, Richard J.; Feldman, Brian M.; Harris-Love, Michael O.; Koontz, Diane C.; Fertig, Noreen; Kelley, Stephanie S.; Pryber, Sherrie L.; Miller, Frederick W.; Rockette, Howard E. (February 2013). "Rituximab in the treatment of refractory adult and juvenile dermatomyositis and adult polymyositis: a randomized, placebo-phase trial". Arthritis and Rheumatism. 65 (2): 314–324. doi:10.1002/art.37754. ISSN 1529-0131. PMC 3558563. PMID 23124935.
  55. ↑ Paik, Julie J.; Casciola-Rosen, Livia; Shin, Joseph Yusup; Albayda, Jemima; Tiniakou, Eleni; Leung, Doris G.; Gutierrez-Alamillo, Laura; Perin, Jamie; Florea, Liliana; Antonescu, Corina; Leung, Sherry G.; Purwin, Grazyna; Koenig, Andrew; Christopher-Stine, Lisa (May 2021). "Study of Tofacitinib in Refractory Dermatomyositis: An Open-Label Pilot Study of Ten Patients". Arthritis & Rheumatology (Hoboken, N.J.). 73 (5): 858–865. doi:10.1002/art.41602. ISSN 2326-5205. PMC 8084900. PMID 33258553.
  56. ↑ Hornung, Thorsten; Janzen, Viktor; Heidgen, Franz-Josef; Wolf, Dominik; Bieber, Thomas; Wenzel, Joerg (2014-12-25). "Remission of Recalcitrant Dermatomyositis Treated with Ruxolitinib". New England Journal of Medicine. 371 (26): 2537–2538. doi:10.1056/NEJMc1412997. ISSN 0028-4793. PMID 25539124.
  57. ↑ Ladislau, Leandro; Suárez-Calvet, Xavier; Toquet, Ségolène; Landon-Cardinal, Océane; Amelin, Damien; Depp, Marine; Rodero, Mathieu P; Hathazi, Denisa; Duffy, Darragh; Bondet, Vincent; Preusse, Corinna; Bienvenu, Boris; Rozenberg, Flore; Roos, Andreas; Benjamim, Claudia F (2018-05-08). "JAK inhibitor improves type I interferon induced damage: proof of concept in dermatomyositis". Brain. 141 (6): 1609–1621. doi:10.1093/brain/awy105. ISSN 0006-8950. PMID 29741608.
  58. ↑ Kim, Hanna; Dill, Samantha; O'Brien, Michelle; Vian, Laura; Li, Xiaobai; Manukyan, Manuk; Jain, Minal; Adeojo, Lilian W.; George, Jomy; Perez, Maria; Grom, Alexei A.; Sutter, Michelle; Feldman, Brian M.; Yao, Lawrence; Millwood, Michelle (March 2021). "Janus kinase (JAK) inhibition with baricitinib in refractory juvenile dermatomyositis". Annals of the Rheumatic Diseases. 80 (3): 406–408. doi:10.1136/annrheumdis-2020-218690. ISSN 1468-2060. PMC 7904969. PMID 32843325.
  59. ↑ Vleugels, Ruth Ann; Paik, Julie J.; Bauer Ventura, Iazsmin; Mangold, Aaron R.; Gandiga, Prateek C.; Haemel, Anna; Chinoy, Hector; Hussain, Yessar M.; Sivakumar, Kumaraswamy; Griger, Zoltan; Lee, Eun Bong; Bozan, Francisca; Hsu, Chung-Yuan; Femia, Alisa; Dimachkie, Mazen M. (2026-05-14). "A Phase 3 Trial of Brepocitinib in Dermatomyositis". The New England Journal of Medicine. 394 (19): 1883–1893. doi:10.1056/NEJMoa2503531. ISSN 1533-4406. PMID 41910335.
  60. ↑ Fiorentino, David; Mangold, Aaron R.; Werth, Victoria P.; Christopher-Stine, Lisa; Femia, Alisa; Chu, Myron; Musiek, Amy C. M.; Sluzevich, Jason C.; Graham, Lauren V.; Fernandez, Anthony P.; Aggarwal, Rohit; Rieger, Kerri; Page, Karen M.; Li, Xingpeng; Hyde, Craig (2025-01-11). "Efficacy, safety, and target engagement of dazukibart, an IFNβ specific monoclonal antibody, in adults with dermatomyositis: a multicentre, double-blind, randomised, placebo-controlled, phase 2 trial". Lancet (London, England). 405 (10473): 137–146. doi:10.1016/S0140-6736(24)02071-3. ISSN 1474-547X. PMID 39798982.
  61. ↑ Müller, Fabian; Taubmann, Jule; Bucci, Laura; Wilhelm, Artur; Bergmann, Christina; Völkl, Simon; Aigner, Michael; Rothe, Tobias; Minopoulou, Ioanna; Tur, Carlo; Knitza, Johannes; Kharboutli, Soraya; Kretschmann, Sascha; Vasova, Ingrid; Spoerl, Silvia (2024-02-21). "CD19 CAR T-Cell Therapy in Autoimmune Disease — A Case Series with Follow-up". New England Journal of Medicine. 390 (8): 687–700. doi:10.1056/NEJMoa2308917. ISSN 0028-4793. PMID 38381673.
  62. ↑ Müller, Fabian; Wirsching, Andreas; Hagen, Melanie; Völkl, Simon; Tur, Carlo; Raimondo, Maria Gabriella; Taubmann, Jule; Bucci, Laura; Zhang, Liang; Kretschmann, Sascha; Aigner, Michael; Eckstein, Markus; Spörl, Silvia; Kharboutli, Soraya; Böltz, Sebastian (June 2025). "BCMA CAR T cells in a patient with relapsing idiopathic inflammatory myositis after initial and repeat therapy with CD19 CAR T cells". Nature Medicine. 31 (6): 1793–1797. doi:10.1038/s41591-025-03718-3. ISSN 1546-170X. PMC 12176613. PMID 40245922.
  63. ↑ Hagen, Melanie; Bucci, Laura; Böltz, Sebastian; Nöthling, Danae-Mona; Rothe, Tobias; Anoshkin, Kirill; Raimondo, Maria G.; Tur, Carlo; Wirsching, Andreas; Wacker, Jochen; Düsing, Christina; Distler, Jörg H. W.; Kuwert, Torsten; Bozec, Aline; Ramming, Andreas (2024-09-04). "BCMA-Targeted T-Cell–Engager Therapy for Autoimmune Disease". New England Journal of Medicine. 391 (9): 867–869. doi:10.1056/NEJMc2408786. ISSN 0028-4793. PMID 39231353.
  64. ↑ Chinoy, H.; Rodriguez-Garcia, S.; Neto, A.; Papadopoulou, D.; Baelen, B. Van; Duncombe, P.; Ceuninck, L. De; Woning, B. van der; Aggarwal, R. (2025-06-01). "Op0002 Efficacy and Safety of Efgartigimod Ph20 Sc in Adult Participants with Active Idiopathic Inflammatory Myopathy: Phase 2 Results from the Alkivia Study". Annals of the Rheumatic Diseases. 84: 2–3. doi:10.1016/j.ard.2025.05.025. ISSN 0003-4967.
  65. ↑ Badrising, Umesh A.; Maat-Schieman, Marion L. C.; Ferrari, Michel D.; Zwinderman, Aeilko H.; Wessels, Judith A. M.; Breedveld, Ferdinand C.; van Doorn, Pieter A.; van Engelen, Baziel G. M.; Hoogendijk, Jessica E.; Höweler, Chris J.; de Jager, Aeiko E.; Jennekens, Frans G. I.; Koehler, Peter J.; de Visser, Marianne; Viddeleer, Alain (March 2002). "Comparison of weakness progression in inclusion body myositis during treatment with methotrexate or placebo". Annals of Neurology. 51 (3): 369–372. doi:10.1002/ana.10121. ISSN 0364-5134. PMID 11891832.
  66. ↑ "Therapy for inclusion body myositis | Cochrane". www.cochrane.org. Retrieved 2026-06-30.
  67. ↑ Dalakas, Marinos C.; Rakocevic, Goran; Schmidt, Jens; Salajegheh, Mohammad; McElroy, Beverly; Harris-Love, Michael O.; Shrader, Joseph A.; Levy, Ellen W.; Dambrosia, James; Kampen, Robert L.; Bruno, David A.; Kirk, Allan D. (June 2009). "Effect of Alemtuzumab (CAMPATH 1-H) in patients with inclusion-body myositis". Brain: A Journal of Neurology. 132 (Pt 6): 1536–1544. doi:10.1093/brain/awp104. ISSN 1460-2156. PMC 2685923. PMID 19454532.
  68. ↑ Amato, Anthony A.; Hanna, Michael G.; Machado, Pedro M.; Badrising, Umesh A.; Chinoy, Hector; Benveniste, Olivier; Karanam, Ananda Krishna; Wu, Min; Tankó, László B.; Schubert-Tennigkeit, Agnes Annette; Papanicolaou, Dimitris A.; Lloyd, Thomas E.; Needham, Merrilee; Liang, Christina; Reardon, Katrina A. (2021-03-23). "Efficacy and Safety of Bimagrumab in Sporadic Inclusion Body Myositis: Long-term Extension of RESILIENT". Neurology. 96 (12): e1595–e1607. doi:10.1212/WNL.0000000000011626. ISSN 1526-632X. PMC 8032371. PMID 33597289.
  69. ↑ Benveniste, Olivier; Hogrel, Jean-Yves; Belin, Lisa; Annoussamy, Mélanie; Bachasson, Damien; Rigolet, Aude; Laforet, Pascal; Dzangué-Tchoupou, Gaëlle; Salem, Joe-Elie; Nguyen, Lee S.; Stojkovic, Tanya; Zahr, Noel; Hervier, Baptiste; Landon-Cardinal, Océane; Behin, Anthony (January 2021). "Sirolimus for treatment of patients with inclusion body myositis: a randomised, double-blind, placebo-controlled, proof-of-concept, phase 2b trial". The Lancet. Rheumatology. 3 (1): e40–e48. doi:10.1016/S2665-9913(20)30280-0. ISSN 2665-9913. PMID 38273639.
  70. ↑ Machado, Pedro M.; McDermott, Michael P.; Blaettler, Thomas; Sundgreen, Claus; Amato, Anthony A.; Ciafaloni, Emma; Freimer, Miriam; Gibson, Summer B.; Jones, Sarah M.; Levine, Todd D.; Lloyd, Thomas E.; Mozaffar, Tahseen; Shaibani, Aziz I.; Wicklund, Matthew; Rosholm, Anders (October 2023). "Safety and efficacy of arimoclomol for inclusion body myositis: a multicentre, randomised, double-blind, placebo-controlled trial". The Lancet. Neurology. 22 (10): 900–911. doi:10.1016/S1474-4422(23)00275-2. ISSN 1474-4465. PMID 37739573.
  71. ↑ "Abcuro Presents Results from Phase 2/3 MUSCLE Study of Ulviprubart in Patients with Inclusion Body Myositis at GCOM 2026". Abcuro. 2026-03-26. Retrieved 2026-06-30.
  72. ↑ Anderson, Nicolaas C.; Lloyd, Thomas E. (2025-01-01). "Inclusion body myositis: an update". Current Opinion in Rheumatology. 37 (1): 80–85. doi:10.1097/BOR.0000000000001060. ISSN 1531-6963. PMID 39469805.
  73. ↑ Spector SA, Lemmer JT, Koffman BM, Fleisher TA, Feuerstein IM, Hurley BF, Dalakas MC (October 1997). "Safety and efficacy of strength training in patients with sporadic inclusion body myositis". Muscle & Nerve. 20 (10): 1242–1248. doi:10.1002/(sici)1097-4598(199710)20:10<1242::aid-mus6>3.3.co;2-x. PMID 9324080. Cited in:
    • Dalakas, Marinos C (08 September 2010). "Treatment and Management of Autoimmune Myopathies". In Bertorini, Tulio E. Neuromuscular Disorders. Elsevier Health Sciences. pp. 395—408. ISBN 9781437703726
  74. ↑ Dalakas MC (8 September 2010). "Treatment and Management of Autoimmune Myopathies". In Bertorini TE (ed.). Neuromuscular Disorders. Elsevier Health Sciences. pp. 395–408. ISBN 978-1-4377-0372-6.
  75. ↑ Baer AN, Wortmann RL (May 2013). "Noninflammatory myopathies". Rheumatic Disease Clinics of North America. 39 (2): 457–479. doi:10.1016/j.rdc.2013.02.006. PMID 23597974.
  76. ↑ Michelle, E. Harlan; Mammen, Andrew L. (October 2015). "Myositis Mimics". Current Rheumatology Reports. 17 (10): 63. doi:10.1007/s11926-015-0541-0. ISSN 1534-6307. PMC 13209152. PMID 26290112.
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