The early kinetics of cytomegalovirus-specific CD8⁺ T cell responses are not affected by antigen load or the absence of perforin or IFN-

Immunology and Virology Program, Centre for Ophthalmology and Visual Science, The University of Western Australia, Western Australia, Australia; Centre for Experimental Immunology, Lions Eye Institute, Nedlands, Western Australia, Australia; Cancer Immunology Program, Sir Donald and Lady Trescowthick Laboratories, Peter MacCallum Cancer Centre, East Melbourne 3002, Victoria, Australia

^* To whom correspondence should be addressed. Email: mariapia{at}cyllene.uwa.edu.a.

	Abstract

Both innate and adaptive immune responses participate in the control of murine cytomegalovirus (mCMV) infection. In some mouse strains, like BALB/c, the control of infection relies principally on the activities of CD8⁺ T cells. mCMV-specific CD8⁺ T cell responses are unusual in that, even after mCMV has been controlled in the periphery, the number of circulating virus-specific CD8⁺ T cells remains high compared to those observed in other viral infections. To better understand the generation and maintenance of mCMV-specific CD8⁺ T cell responses, we evaluated how antigen load and effector molecules, such as perforin (Prf) and IFN-, influence these responses during acute infection in vivo. Viral burden affected the magnitude, but not the early kinetics of antigen-specific CD8⁺ T cell responses. Similarly, the magnitude of virus-specific CD8⁺ T cell expansion was affected by Prf and IFN-, but contraction of antigen-specific responses occurred normally in both Prf and IFN- deficient mice. These data indicate that control of mCMV-specific CD8⁺ T cell expansion and contraction is more complex than anticipated and, despite the role of Prf or IFN- in controlling viral replication, a full program of T cell expansion and contraction can occur in their absence.