Inhibition of IL-17 ameliorates systemic lupus erythematosus in Roquin^san/san mice through regulating the balance of TFH cells, GC B cells, Treg and Breg.

ABSTRACT: Systemic lupus erythematosus (SLE) is mediated by a chronic and dysregulated inflammatory response. Interleukin (IL)-17, a proinflammatory cytokine, and T helper (Th)17 cells are associated with chronic autoimmune diseases. We hypothesized that inhibition of IL-17 would decrease the numbers of T cell subsets that function as B-cell helpers, as well as B-cell differentiation into plasma cells and autoantibody expression. The IL-17 level was increased markedly in Roquin^san/san mice. Loss of IL-17 in Roquin^san/san mice improved nephritis by downregulating immunoglobulin (Ig)G, IgG1, and IgG2a production. Formation of germinal centers (GCs), and follicular B- and T-cell differentiation was reduced, whereas the number of regulatory T (Treg) cells and immature B cells was i

SUBMITTER: Lee SY 

PROVIDER: S-EPMC6435653 | biostudies-literature | 2019 Mar

REPOSITORIES: biostudies-literature