TY - JOUR
T1 - The role of γδ T cells in induction of bacterial antigen-specific protective CD8+ cytotoxic T cells in immune response against the intracellular bacteria Listeria monocytogenes
AU - Nomura, A.
AU - Matsuzaki, G.
AU - Takada, H.
AU - Hiromatsu, K.
AU - Nabeshima, S.
AU - Nakamura, T.
AU - Kishihara, K.
AU - Nomoto, K.
N1 - Copyright:
Copyright 2004 Elsevier Science B.V., Amsterdam. All rights reserved.
PY - 1998
Y1 - 1998
N2 - The role of T-cell receptor (TCR) γβ T cells in the induction of protective TCR αβ T cells against infection by the intracellular bacteria Listeria monocytogenes was analysed. We found that depletion of γδ T cells by anti-TCR δ monoclonal antibody treatment before intravenous immunization of mice with a sublethal dose of viable L. monoeytogenes resulted in reduction of protection against secondary challenge infection in the immunized mice. The γδ T-cell depletion also reduced induction of protective αβ T cells capable of transferring the protection against challenge infection of L. monocytogenes into naive mice. Furthermore, the protective T cells that were affected by the γδ T-cell depletion were suggested to be CD8+ cytotoxic T cells rather than CD4+ T cells by the following observations. First, induction of cytotoxic T lymphocytes specific to a L. monocytogenes-derived H-2K(d)-restricted peptide (listeriolysin O 91- 99) was significantly suppressed by γδ T-cell depletion before immunization. Second, γδ T-cell depletion did not affect cytokine production and proliferation of T cells from immunized mice in response to in vitro stimulation with heat-killed Listeria which preferentially stimulates CD4+ T cells. Third, CD8+ αβ T cells from control immunized mice transferred protection against infection of L. monocytogenes into naive mice but only a limited degree of protection was transferred by CD8+ T cells from the γδ T-cell-depleted immunized mice; and fourth, CD4+ αβ T cells from the γδb T-cell-depleted mice transferred a similar level of protection as those from the control immunized mice. All these results suggest that γδ T cells participate in establishment of protective immunity against intracellular bacteria by supporting priming of bacterial antigen-specific CD8+ cytotoxic T cells.
AB - The role of T-cell receptor (TCR) γβ T cells in the induction of protective TCR αβ T cells against infection by the intracellular bacteria Listeria monocytogenes was analysed. We found that depletion of γδ T cells by anti-TCR δ monoclonal antibody treatment before intravenous immunization of mice with a sublethal dose of viable L. monoeytogenes resulted in reduction of protection against secondary challenge infection in the immunized mice. The γδ T-cell depletion also reduced induction of protective αβ T cells capable of transferring the protection against challenge infection of L. monocytogenes into naive mice. Furthermore, the protective T cells that were affected by the γδ T-cell depletion were suggested to be CD8+ cytotoxic T cells rather than CD4+ T cells by the following observations. First, induction of cytotoxic T lymphocytes specific to a L. monocytogenes-derived H-2K(d)-restricted peptide (listeriolysin O 91- 99) was significantly suppressed by γδ T-cell depletion before immunization. Second, γδ T-cell depletion did not affect cytokine production and proliferation of T cells from immunized mice in response to in vitro stimulation with heat-killed Listeria which preferentially stimulates CD4+ T cells. Third, CD8+ αβ T cells from control immunized mice transferred protection against infection of L. monocytogenes into naive mice but only a limited degree of protection was transferred by CD8+ T cells from the γδ T-cell-depleted immunized mice; and fourth, CD4+ αβ T cells from the γδb T-cell-depleted mice transferred a similar level of protection as those from the control immunized mice. All these results suggest that γδ T cells participate in establishment of protective immunity against intracellular bacteria by supporting priming of bacterial antigen-specific CD8+ cytotoxic T cells.
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U2 - 10.1046/j.1365-2567.1998.00593.x
DO - 10.1046/j.1365-2567.1998.00593.x
M3 - Article
C2 - 9824480
AN - SCOPUS:0031593642
VL - 95
SP - 226
EP - 233
JO - Immunology
JF - Immunology
SN - 0019-2805
IS - 2
ER -