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Infection and Immunity, December 2004, p. 6884-6891, Vol. 72, No. 12
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.12.6884-6891.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Bystander Activation of CD8+ T Lymphocytes during Experimental Mycobacterial Infection

Brad Gilbertson,1 Susie Germano,1 Pauline Steele,1,{dagger} Steven Turner,1 Barbara Fazekas de St. Groth,2 and Christina Cheers1*

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-{gamma})-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-{gamma}-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 CD44hi (memory phenotype) T cells. The transferred CD8+ T cells proliferated in vivo, although this was not essential for IFN-{gamma} 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.

* Corresponding author. Mailing address: Department of Microbiology and Immunology, University of Melbourne, Victoria 3010, Australia. Phone: 61 3 8344 5708. Fax: 61 3 9347 1540. E-mail: ccheers{at}unimelb.edu.au.

Editor: J. D. Clements

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

Infection and Immunity, December 2004, p. 6884-6891, Vol. 72, No. 12
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.12.6884-6891.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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