DNA microarray analysis of the gene expression profiles of naive versus activated tumor-specific T cells

DNA microarray analysis of the gene expression profiles of naive versus activated tumor-specific T cells
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DOI:
10.1016/s0024-3205(02)02164-1
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发表时间:
2002-11-08
期刊:
影响因子:
6.1
通讯作者:
Xiang, J
Xiang, J
中科院分区:
医学2区
文献类型:
--
作者:
Zhang, XS;Chen, ZA;Xiang, J

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T cells are a key element in effective cancer immunity, recognizing MHC-antigen peptide complexes on the surface of antigen presenting cells and translating these signals into cytotoxic effector T cell responses. In this study, we systematically investigated by DNA array analysis the expression profiles of 514 immunologically relevant genes in naive and SP2/0 tumor-specific activated mouse T cell populations. Our data shows that naive T cells expressed 37 (i.e., 7.6% of the 514) transcripts with expression level (EL) values of greater than or equal to 2.0, while the activated T cells expressed 101 such transcripts. The expression levels of 9 (1.75% of 514) of the shared transcripts were equivalent in the two populations of T cells. Ninety-six genes were differently expressed upon T cell activation, with 71 (13.81%) being up-regulated and 25 (4.86%) down-regulated. The list of significantly affected genes includes numerous cytokines and their receptors (e.g., IL-2Ralpha, IL-6Ralpha, IL-7Ralpha, IL-16, IL-17R, TGF-beta), chemokines and chemokine receptors (e.g., RANTES, CCR7, CXCR4), alternate surface proteins (e.g., 4-IBB, GITR, integrins-alphaL and -beta7, L-selectin, CD6, CD45 and EMMPRIN), cytoplasmic signaling intermediates (e,g., GATA-3, 14-3-3-eta, CIS1, SMAD4 and JAK1) and an array of other molecules (e.g., NFkappa-B inducing kinase, LTBP3 and persephin), several of which are associated with Th1 responses, and T cell self-regulation or migration. Taken together, our data contribute to our understanding of the generalized processes that accompany T cell activation and, more specifically, to our understanding of the processes associated with T cell activation during antitumor responses. (C) 2002 Published by Elsevier Science Inc.