Germinal centers (GC) are essential for an effective humoral immune response. The GC provides an environment that stimulates B cells to proliferate in response to antigens and accumulate somatic mutations in immunoglobulin (Ig) genes, with help from T follicular helper (Tfh) cells, leading to affinity maturation of antigen specific antibodies. Although much work over the last decades has accumulated in this field, several mechanisms still remain unclear. This project investigates the role of CXCL12/heparan sulfate interactions in the function of this chemokine. These interactions immobilize the chemokine, promoting gradient formation. For this purpose, we study mice that carry a mutant CXCL12 molecule (KI), where interactions with the extracellular matrix are abrogated.
This project intends to analyze the consequences of lack of interaction between CXCL12/heparan sulfate (HS) on gene expression profiles on germinal center B cells in spleen, and infer about the role of these interactions on humoral immune response.