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The Journal of Immunology, 1999, 162: 4910-4913.
Copyright © 1999 by The American Association of Immunologists

Inflammation Alone Evokes the Response of a TCR-Invariant Mouse {gamma}{delta} T Cell Subset1

Akiko Mukasa2,*, Willi K. Born*,{dagger} and Rebecca L. O’Brien3,*,{dagger}

* National Jewish Medical and Research Center, Denver, CO 80206; and {dagger} Department of Immunology, University of Colorado Health Sciences Center, Denver, CO 80262

Whether {gamma}{delta} T lymphocytes respond to microbial Ags or to inducible host Ags remains a matter of controversy. Using several different disease models and mouse strains, we and others have seen that V{gamma}6/V{delta}1 {gamma}{delta} T cells preferentially increase among the {gamma}{delta} T cells infiltrating inflamed tissues. However, it was not clear whether bacteria are necessary to bring about this response. Therefore, we have reexamined this question using a disease model in which inflammation is induced by a purely autoimmune process involving no bacteria, bacterial products, or other foreign material: testicular cell-induced autoimmune orchitis. Using this model we found that {gamma}{delta} T cells were still plentiful among the infiltrating T lymphocytes, being 9- to 10-fold more prevalent than in spleen, and that V{gamma}6/V{delta}1+ cells again represented the predominant {gamma}{delta} T cell type. This finding shows that the response of the V{gamma}6/V{delta}1+ subset does not, in fact, depend upon the presence of bacteria or bacterial products. The stimulus triggering the response of the V{gamma}6/V{delta}1 {gamma}{delta} T cells appears to be neither foreign nor organ-specific in origin, but instead consists of a self-derived host Ag or signal induced during the inflammatory process.




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