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Bystander Activation of CD8⁺ T Lymphocytes during Experimental Mycobacterial Infection

Brad Gilbertson,¹ Susie Germano,¹ Pauline Steele,^1, Steven Turner,¹ Barbara Fazekas de St. Groth,² and Christina Cheers^1*

Department of Microbiology and Immunology, University of Melbourne, Victoria,¹ Centenary Institute of Cancer Medicine and Cell Biology, Newtown, New South Wales, Australia²

Received 15 June 2004/ Returned for modification 21 July 2004/ Accepted 22 August 2004

Infection of C57BL/6 mice with Mycobacterium avium leads to the activation of both CD4⁺ and CD8⁺ gamma interferon (IFN-)-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--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- 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.

Editor: J. D. Clements

Present address: The Macfarlane Burnet Institute for Medical Research and Public Health, Melbourne, Victoria 3001, Australia.

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