When humans are exposed to a substance that causes an immune response, to protect the itself, the body generates antibodies. There is very little understood about the role of chemokines in regulating the extent of the immune response, as measured by antibody titers and types of antibodies that are made. We have found that C-C chemokine receptor 7 regulates the antibody titers by controlling the localization of different populations of immune cells to the bone marrow. In this proposal our goal is to better understand the molecular mechanisms that are employed by immune T cells to respond to C-C chemokine receptor 7 activation that regulate the targeting of T cells to the bone marrow where they regulate the isotype switching and antibody production by immune cells. Our study is important since these antibodies protect the host when he or she is exposed to the same substance during a secondary immune response. We hypothesize that CCR7 regulates the migration of memory T, and regulatory T cells to the bone marrow to limit the activation of B cells during an adaptive immune response. With the knowledge we gain we will determine if redirection of the T cells can be applied to inhibit excessive immune responses observed during autoimmune diseases.
Chemokine receptors, are cell surface proteins that direct cells to different sites within the body. We have shown that one of these receptors CC Chemokine receptor 7 is limits the extent of the immune response, to prevent an excessive response as is seen with autoimmune disease. This proposal will extend our work on the immune system, to better understand how CC Chemokine receptor 7 regulated patterning of cells in a human prevents an excessive immune response.
