Intracellular signals of T cell costimulation

被引:55
作者
Song, Jianxun [1 ,2 ]
Lei, Fengyang Tylan [1 ,2 ]
Xiong, Xiaofang [1 ,2 ]
Haquel, Rizwanul [1 ,2 ]
机构
[1] Penn State Univ, Coll Med, Dept Microbiol & Immunol, Hershey, PA 17033 USA
[2] Penn State Univ, Coll Med, Penn State Canc Inst, Hershey, PA 17033 USA
关键词
costimulation; signal transduction; T-cell development;
D O I
10.1038/cmi.2008.30
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Ligation of T cell receptor (TCR) alone is insufficient to induce full activation of T lymphocytes. Additional ligand-receptor interactions (costimulation) on antigen presenting cells (APCs) and T cells are required. T cell costimulation has been shown to be essential for eliciting efficient T cell responses, involving all phases during T cell development. However, the mechanisms by which costimulation affects the function of T cells still need to be elucidated. In recent years, advances have been made in studies of costimulation as potential therapies in cancer, infectious disease as well as autoimmune disease. In this review, we discussed intracellular costimulation signals that regulate T cell proliferation, cell cycle progression, cytokine production, survival, and memory development. In general, the pathway of phosphoinositide-3 kinase (PI3K)/protein kinase B (PKB, also known as Akt)/nuclear factor kappa B (NF-kappa B) might be central to many costimulatory effects. Through these pathways, costimulation controls T-cell expansion and proliferation by maintenance of survivin and aurora B expression, and sustains long-term T-cell survival and memory development by regulating the expression of bcl-2 family members.
引用
收藏
页码:239 / 247
页数:9
相关论文
共 92 条
[1]   The Noxa/Mcl-1 axis regulates susceptibility to apoptosis under glucose limitation in dividing T cells [J].
Alves, Nuno L. ;
Derks, Ingrid A. M. ;
Berk, Erik ;
Spijker, Rene ;
van Lier, Rene A. W. ;
Eldering, Eric .
IMMUNITY, 2006, 24 (06) :703-716
[2]   TH17 cells contribute to uveitis and scleritis and are expanded by IL-2 and inhibited by IL-27/STAT1 [J].
Amadi-Obi, Ahjoku ;
Yu, Cheng-Rong ;
Liu, Xuebin ;
Mahdi, Rashid M. ;
Clarke, Grace Levy ;
Nussenblatt, Robert B. ;
Gery, Igal ;
Lee, Yun Sang ;
Egwuagu, Charles E. .
NATURE MEDICINE, 2007, 13 (06) :711-718
[3]   CD28 ligation in the absence of TCR promotes ReIA/NF-κB recruitment and trans-activation of the HIV-1 LTR [J].
Annibaldi, Alessandro ;
Sajeva, Angela ;
Muscolini, Michela ;
Ciccosanti, Fabiola ;
Corazzari, Marco ;
Piacentini, Mauro ;
Tuosto, Loretta .
EUROPEAN JOURNAL OF IMMUNOLOGY, 2008, 38 (05) :1446-1451
[4]   CD28 costimulation mediates transcription of SKP2 and CKS1, the substrate recognition components of SCFSkp2 ubiquitin ligase that leads p27kip1 to degradation [J].
Appleman, Leonard J. ;
Chernova, Irene ;
Li, Lequn ;
Boussiotis, Vassiliki A. .
CELL CYCLE, 2006, 5 (18) :2123-2129
[5]   CD28 costimulation mediates down-regulation of p27kip1 and cell cycle progression by activation of the PI3K/PKB signaling pathway in primary human T cells [J].
Appleman, LJ ;
van Puijenbroek, AAFL ;
Shu, KM ;
Nadler, LM ;
Boussiotis, VA .
JOURNAL OF IMMUNOLOGY, 2002, 168 (06) :2729-2736
[6]  
Arestides RSS, 2002, EUR J IMMUNOL, V32, P2874, DOI 10.1002/1521-4141(2002010)32:10<2874::AID-IMMU2874>3.0.CO
[7]  
2-4
[8]   PKCθ signals activation versus tolerance in vivo [J].
Berg-Brown, NN ;
Gronski, MA ;
Jones, RG ;
Elford, AK ;
Deenick, EK ;
Odermatt, B ;
Littman, DR ;
Ohashi, PS .
JOURNAL OF EXPERIMENTAL MEDICINE, 2004, 199 (06) :743-752
[9]  
Biswas DK, 2003, CANCER RES, V63, P290
[10]   CD28 costimulatory signal induces protein arginine methylation in T cells [J].
Blanchet, F ;
Cardona, A ;
Letimier, FA ;
Hershfield, MS ;
Acuto, O .
JOURNAL OF EXPERIMENTAL MEDICINE, 2005, 202 (03) :371-377