LFA-1-deficient mice show normal CTL responses to virus but fail to reject immunogenic tumor.

Rudolf Schmits(Ontario Institute for Cancer Research), Thomas M. Kündig(Ontario Institute for Cancer Research), D. Baker(Ontario Institute for Cancer Research), G Shumaker(Ontario Institute for Cancer Research), John Simard(Ontario Institute for Cancer Research), G S Duncan(Ontario Institute for Cancer Research), Andrew Wakeham(Ontario Institute for Cancer Research), Arda Shahinian(Ontario Institute for Cancer Research), A. van der Heiden(Ontario Institute for Cancer Research), Martin F. Bachmann(Ontario Institute for Cancer Research), Pamela S. Ohashi(Ontario Institute for Cancer Research), Tak W. Mak(Ontario Institute for Cancer Research), DD Hickstein(Ontario Institute for Cancer Research)
The Journal of Experimental Medicine
April 1, 1996
Cited by 278Open Access
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Abstract

The leukocyte integrin LFA-1 (CD11a/CD18) plays an important role in lymphocyte recirculation and homotypic interactions. Leukocytes from mice lacking CD11a displayed defects in in vitro homotypic aggregation, in proliferation in mixed lymphocyte reactions, and in response to mitogen. Mutant mice mounted normal cytotoxic T cell (CTL) responses against systemic LCMV and VSV infections and showed normal ex vivo CTL function. However, LFA-1-deficient mice did not reject immunogenic tumors grafted into footpads and did not demonstrate priming response against tumor-specific antigen. Thus CD11a deficiency causes a selective defect in induction of peripheral immune responses whereas responses to systemic infection are normal.


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