International Immunology, Vol 10, 117-130, Copyright © 1998 by Oxford University Press
Y Kimura, K Yamada, T Sakai, K Mishima, H Nishimura, Y Matsumoto, M Singh and Y Yoshikai
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.
ARTICLES
The regulatory role of heat shock protein 70-reactive CD4+ T cells during rat listeriosis
Laboratory of Host Defense and Germfree Life, Research Institute for Disease Mechanism and Control, Nagoya University School of Medicine, Japan.
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