受到病毒感染后，會產(chǎn)生少量的T 細胞以殺死受到病毒感染的細胞,，這些細胞仍會維持長時間的免疫力,。這些所謂的記憶T 細胞，是來自于CD8 T 細胞的免疫細胞家族,，會進行自我更新的過程,。
這個持續(xù)的過程可以確保免疫系統(tǒng)對抗相同病毒的重復(fù)感染，甚而長達數(shù)十年,。但是并非所有感染都能造成相同的影響,。大部分的病毒可以在幾天或幾星期內(nèi)就從身體清除，但是有些感染,，如HIV或C型肝炎病毒感染等慢性疾病,，就不一樣了。
有些研究建議,，在慢性感染期間產(chǎn)生的病毒特異性CD8 T 細胞,，并不具有急性感染后產(chǎn)生的CD8 T 細胞之特性。
現(xiàn)在,，Wistar研究所的科學(xué)家,，發(fā)現(xiàn)為了對抗慢性感染而產(chǎn)生的CD8 T 細胞，其運作方式與急性感染后產(chǎn)生的CD8 T 細胞不同,，完全依據(jù)病毒是否存在,，來決定這些T細胞的維持。
就研究結(jié)果來看,，免疫系統(tǒng)面對病毒感染時,，會以二種非常不同的細胞類型來反應(yīng)之。在急性感染時,，即使病毒已經(jīng)完全清除,，體內(nèi)仍存在著可以自我更新的記憶T 細胞。但是受到慢性感染時,，則有完全不同的T 細胞,，受到不同的路徑和機制所控制。
此外,，研究結(jié)果也發(fā)現(xiàn),，與慢性感染有關(guān)的CD8 T 細胞，對于IL-7 和IL-15的反應(yīng)不佳,，IL-7 和IL-15是急性感染后,，需要維持記憶T 細胞所需的生長因子,。
因此，慢性感染期間維持的CD8 T 細胞,，建立了一個完全不同的細胞分裂模式,，而可以迅速地轉(zhuǎn)變細胞，這項發(fā)現(xiàn)有助于設(shè)計新的慢性感染疾病之治療方式,。這項研究發(fā)表于4月16 日的The Journal of Experimental Medicine中,。
(資料來源 : Bio.com)
原始出處:
部分英文原文：
Published online 9 April 2007
doi:10.1084/jem.20061937
The Journal of Experimental Medicine, Vol. 204, No. 4, 941-949
© The Rockefeller University Press, 0022-1007 $15.00
Viral antigen and extensive division maintain virus-specific CD8 T cells during chronic infection
Haina Shin1, Shawn D. Blackburn1, Joseph N. Blattman2, and E. John Wherry1
1 Immunology Program, The Wistar Institute, Philadelphia, PA 19104
2 Fred Hutchinson Cancer Research Center, Seattle, WA 98109
CORRESPONDENCE E. John Wherry: jwherry@wistar.org
Efficient maintenance of memory CD8 T cells is central to long-term protective immunity. IL-7– and IL-15–driven homeostatic proliferation is essential for long-term memory CD8 T cell persistence after acute infections. During chronic infections, however, virus-specific CD8 T cells respond poorly to these cytokines. Yet, virus-specific CD8 T cells often persist for long periods of time during chronic infections. We have addressed this apparent paradox by examining the mechanism for maintaining virus-specific CD8 T cells during chronic infection. We find that homeostatic cytokines (e.g., IL-7/15), inflammatory signals, and priming of recent thymic emigrants are not sufficient to maintain virus-specific CD8 T cells over time during chronic infection. Rather, our results demonstrate that viral peptide is required for virus-specific CD8 T cell persistence during chronic infection. Moreover, this viral antigen-dependent maintenance results in a dramatically different type of T cell division than is normally observed during memory T cell homeostasis. Rather than undergoing slow, steady homeostatic turnover during chronic viral infection, CD8 T cells undergo extensive peptide-dependent division, yet cell numbers remain relatively stable. These results indicate that antigen-specific CD8 T cell responses during persisting infection are maintained by a mechanism distinct from that after acute infection.
