The generation and maintenance of CD4+ T cell responses in concomitant immunity to Leishmania major. Sara L Colpitts

ISBN: 9781109227574

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133 pages


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The generation and maintenance of CD4+ T cell responses in concomitant immunity to Leishmania major.  by  Sara L Colpitts

The generation and maintenance of CD4+ T cell responses in concomitant immunity to Leishmania major. by Sara L Colpitts
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Infection with the intracellular protozoan parasite Leishmania major induces a state of concomitant immunity wherein secondary immunity is dependent upon the persistence of the original pathogen. Our lab has described two populations ofMoreInfection with the intracellular protozoan parasite Leishmania major induces a state of concomitant immunity wherein secondary immunity is dependent upon the persistence of the original pathogen.

Our lab has described two populations of Leishmania-induced CD4+ T cells that contribute to immunity: CD62Lhigh central memory T cells and CD62Llow effector T cells. While CD62L downregulation indicates an activated phenotype, a subset of the effector cells has further differentiated into IFN-gamma-producing Th1 effector cells. The factors that result in the generation and maintenance of these populations remain largely unknown during the course of a primary L. major infection. In this thesis, we further examine these populations of CD4+ T cells whose combined efforts mediate rapid protective immunity against secondary L.

major challenge. We used the adoptive transfer of CFSE-labeled transgenic and polyclonal CD4+ T cells to assay the phenotype and function of cells that proliferate in response to L. major infection, and we establish that heterogeneity within the pool of antigen-specific CD4+ T cells arises early following infection.

One of the populations generated at this time had the phenotypic and functional characteristics of central memory T cells. In addition, we demonstrate that the priming of these cells occurs in the draining lymph node in the first 3 days following infection and involves and proliferative arrest of the central memory-like population. In addition, we address a potential mechanism by which Leishmania-specific CD4+ T cells are maintained following infection.

The receptor for the prosurvival cytokine interleukin-7 (IL7R) was expressed at elevated levels on central memory T cells and also a population of Th1-polarized effector T cells suggesting that neither the presence of L. major parasites nor the upregulation of Th1-associated genes prevented the ability of CD4+ T cells to express the IL7R. Moreover, we demonstrate that the rapid effector response to secondary challenge is diminished when IL7R signaling is blocked suggesting a dependence upon IL-7 for the optimal function of Th1 effector cells.

Collectively, the work within this thesis has provided new insights on the early CD4 + T cell response to L. major and the cells that ultimately mediate protective immunity.



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