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Infection and Immunity, May 2007, p. 2244-2252, Vol. 75, No. 5
0019-9567/07/$08.00+0     doi:10.1128/IAI.00024-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Gamma Interferon Responses of CD4 and CD8 T-Cell Subsets Are Quantitatively Different and Independent of Each Other during Pulmonary Mycobacterium bovis BCG Infection

Patricia Ngai, Sarah McCormick, Cherrie Small, Xizhong Zhang, Anna Zganiacz, Naoko Aoki, and Zhou Xing^*

Department of Pathology and Molecular Medicine and Division of Infectious Diseases, Center for Gene Therapeutics, McMaster University, Hamilton, Ontario, Canada

Received 5 January 2007/ Returned for modification 30 January 2007/ Accepted 6 February 2007

Gamma interferon (IFN-) is a key cytokine in host defense against intracellular mycobacterial infection. It has been believed that both CD4 and CD8 T cells are the primary sources of IFN-. However, the relative contributions of CD4 and CD8 T-cell subsets to IFN- production and the relationship between CD4 and CD8 T-cell activation have not been examined. By using a model of pulmonary mycobacterial infection and various immunodetection assays, we found that CD4 T cells mounted a much stronger IFN- response than CD8 T cells at various times after mycobacterial infection, and this pronounced IFN- production by CD4 T cells was attributed to both greater numbers of antigen-specific CD4 T cells and a greater IFN- secretion capacity of these cells. By using major histocompatibility complex class II-deficient or CD4-deficient mice, we found that the lack of CD4 T cells did not negatively affect primary or secondary CD8 T-cell IFN- responses. The CD8 T cells activated in the absence of CD4 T cells were capable of immune protection against secondary mycobacterial challenge. Our results suggest that, whereas both CD4 and CD8 T cells are capable of IFN- production, the former represent a much greater cellular source of IFN-. Moreover, during mycobacterial infection, CD8 T-cell IFN- responses and activation are independent of CD4 T-cell activation.

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* Corresponding author. Mailing address: Rm. 4012-MDCL, Department of Pathology and Molecular Medicine, McMaster University, 1200 Main St. West, Hamilton, Ontario L8N 3Z5, Canada. Phone: (905) 525-9140, ext. 22471. Fax: (905) 522-6750. E-mail: xingz{at}mcmaster.ca

Published ahead of print on 16 February 2007.

Editor: R. P. Morrison

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Infection and Immunity, May 2007, p. 2244-2252, Vol. 75, No. 5
0019-9567/07/$08.00+0     doi:10.1128/IAI.00024-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

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