IL-31 correlates with itch in dermatomyositis
Majid Zeidi
Scholar | Resident Pathology, Dermatopathology
Presented at: International Investigative Dermatology (IID) 2018 Meeting
Date:
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Summary: Dermatomyositis (DM) is an inflammatory myopathy where itch is a major contributor to impaired quality of life. Previously, we have shown that a cytokine responsible for itch in other diseases, interleukin (IL)-31, is elevated in lesional skin of DM patients. We aim to i) demonstrate the correlation between IL-31 and clinical assessment tools and evaluate its strength over time; ii) investigate the variation in IL-31 levels in DM responders vs. non-responders in terms of itch; iii) identify the cellular source of IL-31 in DM. IL-31 expression was quantified using immunohistochemistry (IHC) analysis of lesional skin samples of 12 DM patients at two separate time points. The visual analog scale (VAS), and SKINDEX-29 Symptoms Score clinical assessment tools, and Cutaneous Disease and Activity Severity Index (CDASI) were used to evaluate itch and disease activity. IL-31 expression with respect to mean intensity in lesional skin was highly correlated with SKINDEX-29 Symptoms Score, SKINDEX-29 question 10, and VAS itch score (r=0.85, p<0.001; r=0.77, p<0.01; r=0.68, p<0.05 respectively). IL-31 expression with respect to area stained was highly correlated with CDASI (r=0.78, p<0.01). These correlations were maintained at visit 6 (r=0.65, p<0.05; r=0.64, p<0.05; r=0.60, p<0.05; r=0.74, p<0.01). Responders had a greater reduction of IL-31 relative to non-responders with respect to area stained (p<0.05) and staining intensity (p=0.13). IHC co-localization of lesional skin samples from 4 DM patients at initial presentation was performed to identify the cellular source of IL-31 and revealed co-staining of IL-31 with TH1 T-cells and little or no TH2 production of IL-31. In conclusion, IL-31 plays a key role in DM and is highly correlated with itch and disease severity based on several clinical assessment tools. The responder group had a significant decrease in IL-31 compared to non-responders. The source of IL-31 is likely to be TH1 rather than TH2 cells.