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B Cells Are Required for Generation of Protective Effector and Memory CD4 Cells in Response to Pneumocystis Lung Infection

Frances E. Lund^*, Melissa Hollifield, Kevin Schuer, J. Louise Lines, Troy D. Randall^* and Beth A. Garvy^1,,

^* Trudeau Institute, Saranac Lake, NY 12983; and Department of Microbiology, Immunology, and Molecular Genetics and Division of Infectious Diseases, University of Kentucky, Veterans Affairs Medical Center, Lexington, KY 40536

B cell-deficient mice are susceptible to infection by Pneumocystis carinii f. sp. muris (PC). To determine whether this susceptibility is due to a requirement for B cells to prime T cells, we compared CD4 T cell responses to PC in bone marrow chimeric mice that express MHC class II (MHCII) on all APCs (wild-type (WT) chimeras) and in bone marrow chimeric mice that express MHCII on all APCs except B cells (MHCII^–/– chimeras). Although PC was rapidly cleared by WT chimeric mice, PC levels remained high in chimeric mice that lacked MHCII on B cells. In addition, although T cells were primed in the draining lymph nodes of MHCII^–/– chimeric mice, the number of activated CD4 T cells infiltrating the lungs of these mice was reduced relative to the number in the lungs of WT chimeras. We also adoptively transferred purified CD4 T cells from the draining lymph nodes of PC-infected normal or B cell-deficient mice into SCID mice. Mice that received CD4 cells from normal mice were able to mount a response to infection in the lungs and clear PC. However, mice that received CD4 cells from B cell-deficient mice had a delayed T cell response in the lungs and failed to control the infection. These data indicate that B cells play a vital role in generation of CD4⁺ memory T cells in response to PC infection in the lungs.

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