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Int Immunol. 1998 Feb;10(2):117-30.

The regulatory role of heat shock protein 70-reactive CD4+ T cells during rat listeriosis.

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Laboratory of Host Defense and Germfree Life, Research Institute for Disease Mechanism and Control, Nagoya University School of Medicine, Japan.


Protection against infection with Listeria monocytogenes depends primarily on Listeria-specific T cells. We show here that CD4+ TCR alphabeta+ T cells are capable of recognizing the mycobacterial heat shock protein (HSP) 70, that appears in the peritoneal cavity of F344 rats infected i.p. with L. monocytogenes. The HSP70-reactive CD4+ T cells recognized a peptide comprising 234-252 residues as present in the 70 kDa HSP of Mycobacterium tuberculosis in the context of RT1.B MHC class II molecules. Analysis of TCR Vbeta gene expression with RT-PCR revealed that the HSP70-reactive CD4+ T cells predominantly used the Vbeta16 gene segment, whereas the heat-killed Listeria (HKL)-specific T cells expressed a diverse set of Vbeta gene segments. In contrast to the HKL-specific T cells producing IFN-gamma, the HSP70-reactive CD4+ T cells produced TGF-beta1 and IL-10 but neither Th1- or Th2-type cytokines. Adoptive transfer with HSP70-reactive T cells rendered rats susceptible to listerial infection. Collectively, these results proposed that the HSP70-reactive CD4+ T cells appearing during rat listeriosis may be involved in termination of Th1 cell-mediated excessive inflammation after the battle against L. monocytogenes has been won.

[Indexed for MEDLINE]

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