A CD4⁺ T cell population expanded in lupus blood provides B cell help through interleukin-10 and succinate.

ABSTRACT: Understanding the mechanisms underlying autoantibody development will accelerate therapeutic target identification in autoimmune diseases such as systemic lupus erythematosus (SLE)¹. Follicular helper T cells (T_FH cells) have long been implicated in SLE pathogenesis. Yet a fraction of autoantibodies in individuals with SLE are unmutated, supporting that autoreactive B cells also differentiate outside germinal centers². Here, we describe a CXCR5^-CXCR3⁺ programmed death 1 (PD1)^hiCD4⁺ helper T cell population distinct from T_FH cells and expanded in both SLE blood and the tubulointerstitial areas of individuals with proliferative lupus nephritis. These cells produce interleukin-10 (IL-10) and accumulate mit

SUBMITTER: Caielli S 

PROVIDER: S-EPMC6325012 | biostudies-literature | 2019 Jan

REPOSITORIES: biostudies-literature