Ray Steven J, Franki Suzanne N, Pierce Robert H, Dimitrova Snezhana, Koteliansky Victor, Sprague Andrew G, Doherty Peter C, de Fougerolles Antonin R, Topham David J
Department of Microbiology and Immunology, David H. Smith Center for Vaccine Biology and Immunology, Aab Institute of Biomedical Sciences, University of Rochester, Rochester, NY 14642, USA.
Immunity. 2004 Feb;20(2):167-79. doi: 10.1016/s1074-7613(04)00021-4.
A common feature of many infections is that many pathogen-specific memory T cells become established in diverse nonlymphoid tissues. A mechanism that promotes the retention and survival of the memory T cells in diverse tissues has not been described. Our studies show that the collagen binding alpha1beta1 integrin, VLA-1, is expressed by the majority of influenza-specific CD8 T cells recovered from nonlymphoid tissues during both the acute and memory phases of the response. Antibody treatment or genetic deficiency of VLA-1 decreased virus-specific CTL in the lung and other nonlymphoid tissues, and increased them in the spleen. In spite of the increase in the spleen, secondary heterosubtypic immunity against flu was compromised. This suggests that VLA-1 is responsible for retaining protective memory CD8 T cells in the lung and other tissues via attachment to the extracellular matrix.
许多感染的一个共同特征是，许多病原体特异性记忆T细胞在多种非淋巴组织中得以建立。尚未有促进记忆T细胞在多种组织中滞留和存活的机制被描述。我们的研究表明，胶原结合性α1β1整合素（VLA-1）在应答的急性期和记忆期从非淋巴组织中回收的大多数流感特异性CD8 T细胞中均有表达。VLA-1的抗体处理或基因缺陷会减少肺和其他非淋巴组织中的病毒特异性CTL，并使其在脾脏中增加。尽管脾脏中的CTL有所增加，但针对流感的继发性异源亚型免疫仍受到损害。这表明VLA-1通过附着于细胞外基质负责在肺和其他组织中保留保护性记忆CD8 T细胞。
