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Selected publications
Research statement: Pneumocystis carinii is an opportunistic fungal pathogen that can cause pneumonia in immunosuppressed individuals including AIDS patients. It has been known for a number of years that an intact CD4 T cell compartment is critical for defense against P. carinii. However, there are a number of questions regarding the immune response to P. carinii that are still unresolved. The focus of our work is to examine the immune response to P. carinii using a murine model of infection. There are two major questions that are being addressed:
1. What is the role of B cells in the immune response to P. carinii? It has not been fully appreciated that B cell function is as critical to host defense against P. carinii as is CD4 T cell function. Mice that are deficient in B cells but have normal T cells will succumb to P. carinii pneumonia. Clearly there is a role for P.carinii-specific antibody in clearance of the infection. However, B cells have a variety other of functions such as cytokine production and antigen presentation. We have been using a chimeric mouse model in which we generate mice that have a deficiency in a specific molecule on B cells. We have determined that MHC class II must be present on B cells for clearance of P. carinii. In addition, expression of CD40 on B cells is also required for clearance of the infection. Interestingly, neither MHC class II nor CD40 deficient chimeras were able to produce P. carinii-specific IgG. We are currently using a chimeras, adoptive transfers, and transgenic mice to determine whether B cells are required during early T cell priming events or whether the downstream production of IgG is the major role of B cells in resisting P. carinii infection.
