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

被引:16
作者
Andrews, Daniel M. [1 ,2 ]
Andoniou, Christopher E. [1 ,2 ]
Fleming, Peter [1 ,2 ]
Smyth, Mark J. [3 ]
Degli-Esposti, Mariapia A. [1 ,2 ]
机构
[1] Lions Eye Inst, Ctr Expt Immunol, Nedlands, WA 6009, Australia
[2] Univ Western Australia, Ctr Ophthalmol & Visual Sci, Immunol & Virol Program, Nedlands, WA 6009, Australia
[3] Peter MacCallum Canc Ctr, Canc Immunol Program, Sir Donald & Lady Trescowthick Labs, Melbourne, Vic 3002, Australia
基金
英国惠康基金;
关键词
D O I
10.1128/JVI.02127-07
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Both innate and adaptive immune responses participate in the control of murine cytornegalovirus (mCMV) infection. In some mouse strains, like BALB/c, the control of infection relies 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 numbers of circulating virus-specific CD8(+) T cells remain 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 gamma interferon (IFN-gamma), 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-gamma, but contraction of antigen-specific responses occurred normally in both Prf- and IFN-gamma-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-gamma in controlling viral replication, a full program of T-cell expansion and contraction can occur in their absence.
引用
收藏
页码:4931 / 4937
页数:7
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