TY - JOUR T1 - Peripheral T helper subset profiling in idiopathic inflammatory myositis: Proof of concept JO - ReumatologĂ­a ClĂ­nica T2 - AU - Anuja,Anamika Kumari AU - Mehta,Pankti AU - Singh,Mantabya Kumar AU - Singh,Harshit AU - Nath,Alok AU - Hashim,Zia AU - Khan,Ajmal AU - Gupta,Mansi AU - Misra,Durga P. AU - Agarwal,Vikas AU - Gupta,Latika SN - 1699258X M3 - 10.1016/j.reuma.2022.03.002 DO - 10.1016/j.reuma.2022.03.002 UR - https://reumatologiaclinica.org/es-peripheral-t-helper-subset-profiling-articulo-S1699258X22000705 AB - IntroductionThere is a dearth of biomarkers in Idiopathic Inflammatory Myopathies (IIM) to recognize ongoing muscle inflammation and distinguish damage from activity. Since IIM is an autoantibody-mediated disease with tertiary lymphoid organogenesis reported in the diseased muscles, we aimed to study the peripheral blood T helper (Th) subset profiling as a plausible reflection of ongoing muscle inflammation. MethodsFifty-six patients of IIM were compared with 21 healthy controls (HC) and 18 patients with sarcoidosis. Th1, Th17, Th17.1, and Treg cells were identified after stimulation assays (BD Biosciences). Myositis autoantibodies were tested by line immunoassay (Euroimmune, Germany). ResultsAll Th subsets were elevated in IIM as compared with HC. As compared to HC, PM had elevated Th1 and Treg while Th17 and Th17.1 populations were higher in OM. Patients with sarcoidosis had higher Th1 and Treg but lower Th17 population as compared to IIM {Th1(69.1% vs 49.65%, p<0.0001), {Treg (12.05% vs 6.2%, p<0.0001), {Th17 (2.49% vs 4.4%, p<0.0001)}. Similar results were obtained when sarcoidosis ILD was compared with IIM ILD with a higher Th1 and Treg population but lower Th17 population in the former. No difference in T cell profile was observed after stratification for MSA positivity, type of MSA, clinical features of IIM and disease activity. ConclusionTh subsets in IIM are distinct from sarcoidosis and HC with a TH17 predominant paradigm, creating a case of exploring Th17 pathway and IL-17 blockers for the treatment of IIM. However, cell profiling cannot distinguish active from inactive disease limiting its predictive potential as a biomarker of activity in IIM. ER -