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Role of αβ T cells and γδ T cells in protective immunity to Actinobacillus actinomycetemcomitans in mutant mice by targeted gene disruption
Author(s) -
Takahashi I.,
Nakagawa I.,
Xu L.,
Hamada S.
Publication year - 1996
Publication title -
journal of periodontal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.31
H-Index - 83
eISSN - 1600-0765
pISSN - 0022-3484
DOI - 10.1111/j.1600-0765.1996.tb00524.x
Subject(s) - biology , t cell receptor , t cell , microbiology and biotechnology , antigen , immune system , immunology , hsp60 , heat shock protein , gene , hsp70 , biochemistry
The relative roles of αβ or γδ T cells in protection against Actinobacillus actinomycetemcomitans were analysed by using mutant mice deficient in αβ or γδ T cell receptor (TCR). The dose of A. actinomycetemcomitans producing lethality for the TCR‐α deficient mice was 25% of that for control C57BL/6 mice, while that of TCR‐δ deficient mice was similar to that of C57BL/6 mice. Reverse transcription (RT)‐PCR revealed that γδ T cells from the A. actinomycetemcomitans ‐infected αβ TCR deficient mice expressed significant levels of interferon (IFN)‐γ, interleukin (IL)‐5 and IL‐6 mRNA, whereas αβ T cells from A. actinomycetemcomitans ‐infected γδ TCR deficient mice exhibited significant levels of IFN‐γ and IL‐2 mRNA. Delayed‐type hypersensitivity (DTH) reactions against heat shock protein (HSP) 60 were prominently observed in A. actinomycetemcomitans ‐infected TCR‐δ mutant and C57BL/6 mice, but were absent in TCR‐α mutant mice, suggesting that the DTH response is exclusively dependent on HSP60‐specific αβ T cells producing IFN‐γ and IL‐2 mRNA. It was found that all the mice used exhibited similar levels of serum IgG and IgM responses against A. actinomycetemcomitans ‐specific antigens (whole cells and HSP60), suggesting that αβ as well as γδ T cells participate in the serum immune responses. In addition, the humoral antibody responses displayed in the TCR‐α deficient mice implies resistance to A. actinomycetemcomitans infection. Thus, the resistance to A. actinomycetemcomitans infection may be ascribed mainly to αβ T cells, while γδ T cells can partially compensate for the αβ T cell defect.