Dr. Anna George

Summary of Research:

The broad aim of the research efforts in my laboratory is to understand how systemic and mucosal immune responses are regulated under physiological conditions and under conditions of perturbed homeostasis. Using in vitro, ex vivo and in vivo approaches, and in collaboration with scientists within and outside the institute, we probe the role of cell-intrinsic and cell-extrinsic factors in modulating lymphocyte development and responses, in controlling cell fate determination choices, and in influencing memory/effector pool sizes. We also examine the contribution of innate and adaptive immune components and of microbial factors in determining the severity of experimental colitis. 

Analysis of B cell responses: Our previous data indicate a) thatsignlaing through the TNF receptors CD27 or CD40 during B cell activation inhibits the generation of antibody secreting plasma cells while enhancing the generation of memory cells and b) that a subset of IgM+ “unswitched” memory B cells that expresses CD73 is generated through B cell-T cell interactions involving CD40. We are currently attempting to determine whether CD40-signaling contributes to the maintenance of  the memory and plasma cell pools.

Analysis of T cell responses: We are examining the effect of fever-temperatures maintained during priming on T cell differentiation choices. We are also looking at the contribution of the non-canonical NF-kappaB  pathway in the regulation/maintenance of immune homeostasis and the effect of dietary restriction on T cell development and function.

Role of host and microbial components in experimental colitis: We have found that conventional wildtype mice that differ in IgA responses show differential susceptibility to experimental colitis. We are trying to understand whether IgA affords protection through effects on barrier resilience and/or microbial loads and composition and/or bacterial exclusion.