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*
Laboratory of Host Defense and Germfree Life, Research Institute for Disease Mechanism and Control, Nagoya University School of Medicine, Nagoya, Japan;
Department of Periodontology, School of Dentistry, Aichi-Gakuin University, Chikusa-ku, Nagoya, Japan; and
GBF-German Research Center for Biotechnology, Braunschweig, Germany
We have previously reported that CD4+ T cells
recognizing a peptide comprising residues 234–252 of the heat shock
protein (HSP)70 of Mycobacterium tuberculosis (M.tb) in
the context of RT1.B MHC class II molecule emerged in the peritoneal
cavity during the course of Listeria monocytogenes
infection in rats and suppressed the inflammatory responses against
listerial infection via IL-10 production. We report in this work that
pretreatment with peptide 234–252 of HSP70 derived from
M.tb suppressed the development of adjuvant arthritis
(AA) in Lewis rats induced using heat-killed M.tb. T
cells from rats pretreated with peptide 234–252 produced a significant
amount of IL-10 in response to the epitope. T cells from rats
pretreated with the peptide and immunized with M.tb
produced the larger amount of IL-10 in response to the peptide, but
only a marginal level of IFN-
in response to purified protein
derivative of M.tb. Administration of anti-IL-10 Ab
partly inhibited the suppressive effect of pretreatment with peptide
234–252 on the development of AA. Furthermore, transfer of a T cell
line specific for the epitope at the time of AA induction markedly
suppressed AA. These findings suggested that T cells recognizing
peptide 234–252 may play a regulatory role in inflammation during AA
via the production of suppressive cytokines including
IL-10.
This article has been cited by other articles:
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