Literature DB >> 7907576

A protective role of extrathymic alpha beta TcR cells in the liver in primary murine salmonellosis.

Y Matsumoto1, M Emoto, J Usami, K Maeda, Y Yoshikai.   

Abstract

The liver comprises unique T cells differentiating extrathymically and expressing an intermediate intensity of alpha beta T-cell receptor (TcR) and a high intensity of leucocyte function antigen-1 (LFA-1). To elucidate the functional roles of the intermediate alpha beta TcR cells in host defence against bacterial infection, we examined the effects of depletion of the intermediate alpha beta TcR cells by in vivo administration of monoclonal antibodies (mAb) to intercellular adhesion molecule-1 (ICAM-1)/LFA-1 and alpha beta TcR on the bacterial growth in the liver after infection with Salmonella chorelaesuis in mice. Pretreatment with mAb to LFA-1 (200 micrograms/mouse) together with mAb to ICAM-1 (200 micrograms/mouse), which could preferentially deplete the intermediate alpha beta TcR cells and gamma delta TcR cells in the liver, resulted in a severely reduced ability to resolve acute phase of Salmonella infection in the liver. Pretreatment with a low dose of anti-alpha beta TcR mAb (60 micrograms/mouse), which depleted only bright alpha beta TcR cells, did not affect the bacterial growth in the liver at the early stage after Salmonella infection, while the depleting of both intermediate and bright alpha beta TcR cells by pretreatment with a high dose of anti-alpha beta TcR mAb (120 micrograms/mouse) allowed the bacteria to multiply exaggeratedly in the liver at this stage. These results suggest that intermediate alpha beta TcR cells may play an important role in protection at the early stage after Salmonella infection in liver and that the interaction of ICAM-1/LFA-1 is critically involved in protective roles of extrathymic T cells bearing intermediate alpha beta TcR in liver at the early stage after Salmonella infection.

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Year:  1994        PMID: 7907576      PMCID: PMC1422278     

Source DB:  PubMed          Journal:  Immunology        ISSN: 0019-2805            Impact factor:   7.397


  22 in total

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Review 2.  The lymphocyte function-associated LFA-1, CD2, and LFA-3 molecules: cell adhesion receptors of the immune system.

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Journal:  Annu Rev Immunol       Date:  1987       Impact factor: 28.527

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Journal:  Infect Immun       Date:  1980-01       Impact factor: 3.441

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Authors:  J F Hochadel; K F Keller
Journal:  J Infect Dis       Date:  1977-05       Impact factor: 5.226

5.  Infection breaks T-cell tolerance.

Authors:  M Röcken; J F Urban; E M Shevach
Journal:  Nature       Date:  1992-09-03       Impact factor: 49.962

6.  Comparative efficacy and toxicity of a ribosomal vaccine, acetone-killed cells, lipopolysaccharide, and a live cell vaccine prepared from Salmonella typhhimurium.

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Journal:  Infect Immun       Date:  1978-02       Impact factor: 3.441

7.  Specific acceptance of cardiac allograft after treatment with antibodies to ICAM-1 and LFA-1.

Authors:  M Isobe; H Yagita; K Okumura; A Ihara
Journal:  Science       Date:  1992-02-28       Impact factor: 47.728

8.  Induction of gamma/delta T cells in murine salmonellosis by an avirulent but not by a virulent strain of Salmonella choleraesuis.

Authors:  M Emoto; H Danbara; Y Yoshikai
Journal:  J Exp Med       Date:  1992-08-01       Impact factor: 14.307

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Journal:  J Exp Med       Date:  1969-07-01       Impact factor: 14.307

10.  Cellular resistance to infection.

Authors:  G B MACKANESS
Journal:  J Exp Med       Date:  1962-09-01       Impact factor: 14.307

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  3 in total

1.  Analysis of host cells associated with the Spv-mediated increased intracellular growth rate of Salmonella typhimurium in mice.

Authors:  P A Gulig; T J Doyle; J A Hughes; H Matsui
Journal:  Infect Immun       Date:  1998-06       Impact factor: 3.441

2.  The Salmonella dublin virulence plasmid does not modulate early T-cell responses in mice.

Authors:  L A Guilloteau; A J Lax; S MacIntyre; T S Wallis
Journal:  Infect Immun       Date:  1996-01       Impact factor: 3.441

3.  Recovery from mouse hepatitis virus infection depends on recruitment of CD8(+) cells rather than activation of intrahepatic CD4(+)alphabeta(-)TCR(inter) or NK-T cells.

Authors:  L Lamontagne; S Lusignan; C Page
Journal:  Clin Immunol       Date:  2001-12       Impact factor: 3.969

  3 in total

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