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B cells fail to mature or form LZ despite GC formation in CD19‐deficient mice

Germinal Centers (GC) are crucial to humoral immunity. T cells and follicular dendrtic cells (FDC) work in concert to promote antigen (Ag) specific B cell survival and maturation into antibody forming cells. CD19 is required for proper B cell activation and normal humoral responses. Therefore, we used CD19‐deficient mice to delineate the events leading to GC formation. Mice lacking CD19 do not form GC in the spleen or draining lymph nodes (DLN) in response to SRBC, and as a result, fail to activate FDC in order to receive survival signals. When wild‐type B cells were adoptively transferred into CD19‐deficient mice, GC formation and FDC activation were rescued. In contrast, GC form and FDC are activated in the mesenteric lymph nodes (MLN) of CD19‐deficient mice, presumably due to constant stimulation by Ag. Despite the presence of GC and activated FDC, GC B cells in the MLN of CD19‐deficient mice fail to downregulate IgD and CD38 compared to wild‐type GC B cells, indicating defects in maturation. Furthermore, the light zone (LZ) within these GC is almost nonexistent. Collectively, these results show that splenic and DLN FDC are inactive in CD19‐deficient mice after SBRC challenge, but despite B cell and FDC activation in the MLN of CD19‐deficient mice, CD19 is still required for GC B cells to fully mature and enter the LZ. Supported by NIH R01AI42265.