T-cell exhaustion in HIV infection

被引：78

作者：

El-Far M. ^{[1
]}

Halwani R. ^{[1
]}

Said E. ^{[1
]}

Trautmann L. ^{[1
]}

Doroudchi M. ^{[1
]}

Janbazian L. ^{[1
]}

Fonseca S. ^{[1
]}

Van Grevenynghe J. ^{[1
]}

Yassine-Diab B. ^{[1
]}

Sékaly R.-P. ^{[1
]}

Haddad E.K. ^{[1
]}

机构：

[1] Centre de Recherche du CHUM, Hôpital Saint-Luc, Bureau 1317, Montréal, QC H2X 1P1, 264, René-Lévesque est

来源：

Current HIV/AIDS Reports | 2008年 / 5卷 / 1期

关键词：

Programme Cell Death Ligand; Chronic Viral Infection; Aberrant Immune Response; Dendritic Cell Dysfunction; Chronic LCMV Infection;

D O I：

10.1007/s11904-008-0003-7

中图分类号：

学科分类号：

摘要：

Generation of memory T cells, which mediate immunity against microbes and cancers, relies, for optimal activity, on the interactions of multiple cell types that are highly regulated through the expression of soluble factors and negative and positive receptors. Their disruption will lead to aberrant immune responses, which can result in the invasion of the host by foreign pathogens. In chronic viral infections including HIV and hepatitis C virus, persistence of antigen and lack of CD4 help (HIV) disrupt memory T-cell function and induce defects in memory T-cell responses, which have been defined as T-cell exhaustion. In this review, we examine the molecular mechanisms involved in such T-cell dysfunction. Better understanding of these mechanisms will assist in the development of novel therapies to prevent the immune damage mediated by HIV infection. Copyright © 2008 by Current Medicine Group LLC.

引用

页码：13 / 19

页数：6

共 46 条

[21]

Appay V., Dunbar P.R., Callan M., Et al., Memory CD8+ T cells vary in differentiation phenotype in different persistent virus infections, Nat Med, 8, pp. 379-385, (2002)

[22]

Greenwald R.J., Latchman Y.E., Sharpe A.H., Negative co-receptors on lymphocytes, Curr Opin Immunol, 14, pp. 391-396, (2002)

[23]

Shiratori T., Miyatake S., Ohno H., Et al., Tyrosine phosphorylation controls internalization of CTLA-4 by regulating its interaction with clathrin-associated adaptor complex AP-2, Immunity, 6, pp. 583-589, (1997)

[24]

Chemnitz J.M., Parry R.V., Nichols K.E., Et al., SHP-1 and SHP-2 associate with immunoreceptor tyrosine-based switch motif of programmed death 1 upon primary human T cell stimulation, but only receptor ligation prevents T cell activation, J Immunol, 173, pp. 945-954, (2004)

[25]

Lee K.M., Chuang E., Griffin M., Et al., Molecular basis of T cell inactivation by CTLA-4, Science, 282, pp. 2263-2266, (1998)

[26]

Schneider H., Downey J., Smith A., Et al., Reversal of the TCR stop signal by CTLA-4, Science, 313, pp. 1972-1975, (2006)

[27]

Nishimura H., Honjo T., Minato N., Facilitation of beta selection and modification of positive selection in the thymus of PD-1-deficient mice, J Exp Med, 191, pp. 891-898, (2000)

[28]

Carreno B.M., Collins M., The B7 family of ligands and its receptors: New pathways for costimulation and inhibition of immune responses, Annu Rev Immunol, 20, pp. 29-53, (2002)

[29]

Freeman G.J., Long A.J., Iwai Y., Et al., Engagement of the PD-1 immunoinhibitory receptor by a novel B7 family member leads to negative regulation of lymphocyte activation, J Exp Med, 192, pp. 1027-1034, (2000)

[30]

Fiorentino D.F., Zlotnik A., Mosmann T.R., Et al., IL-10 inhibits cytokine production by activated macrophages, J Immunol, 147, pp. 3815-3822, (1991)

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