Abstract: |
H2-M3-restricted T cells respond more rapidly to primary Listeria monocytogenes infection than conventional MHC class Ia-restricted T cells. Reinfection with L. monocytogenes, while inducing explosive proliferation of H2-Kd-restricted T cells, does not stimulate significant expansion of H2-M3-restricted CTL. These disparate responses to reinfection are apparent within 5 days of primary L. monocytogenes infection. However, H2-M3-restricted memory T cells are generated, and are indistinguishable from classically restricted T cells in terms of cell surface memory markers and longevity. Early responses of H2-M3- and H2-Kd-restricted memory T cells to reinfection are similar, with increases in size and expression of activation markers. Interestingly, priming of H2-M3-restricted T cells with an L. monocytogenes -derived N-formyl peptide plus anti-CD40 generates memory T cells that expand upon re-exposure to Ag during L. monocytogenes infection. Our data indicate that disparate H2-M3- and MHC class Ia-restricted memory T cell responses reflect intrinsic differences between these T cell populations. Although distinct proliferative programs appear to be hardwired in these populations during primary L. monocytogenes infection, under different inflammatory circumstances M3-restricted T cell populations can maintain the ability to expand upon re-exposure to Ag. |
Keywords: |
controlled study; nonhuman; cell proliferation; t lymphocyte; biological markers; animal cell; mouse; animals; mice; cell survival; cell division; animal experiment; animal model; cell population; mice, inbred balb c; mice, inbred c57bl; mice, transgenic; antigen presentation; lymphocyte activation; bacterial protein; cell surface marker; peptide fragments; t-lymphocytes, cytotoxic; histocompatibility antigens class i; t-lymphocyte subsets; memory cell; major histocompatibility complex; immunologic memory; listeriosis; listeria monocytogenes; listeria infections; major histocompatibility antigen class 1; immunization; immunization, secondary; cell surface; antigens, bacterial; heat-shock proteins; bacterial toxins; hemolysin proteins; cd40 ligand monoclonal antibody; reinfection; h-2 antigens; female; priority journal; article; formylpeptide
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