Figure 6

Proposed model showing the effects of venom or isolated proteins on B cell compartment. (A) ASC B220^neg are generated in GC of spleen by a hierarchical process of differentiation in which Bmem starts with high expression of B220 that reach intermediate levels and become ASC negative for this marker in a IL-17A-dependent manner. The longevity of ASC B220^neg in spleen is supported by TLR2 signaling. (B) IL-17A and IL-5 produced by innate cells that depend on TLR2/4 MyD88-signaling directly influences the differentiation and maintenance of ASC B220^neg producing specific-IgG1 on inflamed peritoneal cavity. The longevity of ASC B220^neg is supported by CXCR4 expression dependent on SP1R expression. (C) IL-5 and IL-23 maintain central memory T lymphocytes (TcM) in BM that migrate to secondary lymphoid organs where they could be activated and sustain antibody production by ASC.