Jarid2 Regulates The Function Of Follicular Helper T Cells And Immune Responses

The immune system protects host from invading pathogens and clears tumor cells.The vertebrate immune system is comprised of innate and adaptive immune system.Adaptive immunity can be classified into T cell-mediated cellular immunity and B cell-mediated humoral immunity.The germinal center reaction is the most important physiological process in humoral immunity.Only through germinal center selection,antigen-activated B cells can differentiate into long-lived memory B cells and plasma cells secreting high affinity antibodies.This process is controlled by Follicular helper T cells(TFH).Therefore,the mechanism research of TFH cells differentiation and function are of critical importance for the formation of humoral immunity and immune memory.An increasing number of research indicate that epigenetic modification regulated differentiation of immune cells,immune response and inflammatory diseases.However,there is few research about epigenetic modification in regulating TFH cells differentiation and function.In this study,we firstly explored whether Jarid2 regulates TFH cells differentiation and function and affects the formation of germinal center B cells.We also found Jarid2 regulated histone methylation in activated CD4+T cells.Here we report that mice with T cell-specific deletion of Jarid2 not affected TFH cell differentiation,but germinal center B cell and plasma cell formation were reduced.In addiction,the Jarid2-deficient mice produced less NP-specific IgGl.These results demonstrated that mice with T cell-specific deletion of Jarid2 may impaired function of TFH cells and GC B cell formation through germinal center selection.Meanwhile,we also proved that the levels of H3K27me3 methylation were reduced in Jarid2 deficient CD4+T cells.Therefore,our study reveals that Jarid2 control TFH cells function and immune responses through regulating relevant geneexpressionby modulating H3K27 methylation.