Affiliation:
1. Department of Microbiology and Immunology, University of Melbourne, Victoria
2. Centenary Institute of Cancer Medicine and Cell Biology, Newtown, New South Wales, Australia
Abstract
ABSTRACT
Infection of C57BL/6 mice with
Mycobacterium avium
leads to the activation of both CD4
+
and CD8
+
gamma interferon (IFN-γ)-producing T cells, although the CD8
+
cells play no role in protection against infection. Using transfer of different lines of transgenic T cells with T-cell receptors (TCRs) which recognize irrelevant antigens, we show here that transferred CD8
+
T cells from two of the three lines were activated to the same degree as the host cells, suggesting that the majority of the IFN-γ-producing CD8
+
T cells of the host represented bystander activation. The third line, specific for the male HY antigen, showed no activation. Activation required the participation of the CD28 coreceptor on T cells and was unaffected by the removal of CD44
hi
(memory phenotype) T cells. The transferred CD8
+
T cells proliferated in vivo, although this was not essential for IFN-γ production. Taken together, these data are highly reminiscent of homeostatic proliferation of TCR transgenic T cells upon transfer to lymphopenic hosts, and suggest low-affinity stimulation through the TCR, possibly by self peptides. The findings are discussed in relation to homeostatic proliferation and their significance in the possible induction of autoimmune disease.
Publisher
American Society for Microbiology
Subject
Infectious Diseases,Immunology,Microbiology,Parasitology
Cited by
35 articles.
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