B cells and aging: molecules and mechanisms

被引：150

作者：

Cancro, Michael P. ^{[1
]}

Hao, Yi ^{[1
]}

Scholz, Jean L. ^{[1
]}

Riley, Richard L. ^{[2
]}

Frasca, Daniela ^{[2
]}

Dunn-Walters, Deborah K. ^{[3
]}

Blomberg, Bonnie B. ^{[2
]}

机构：

[1] Univ Penn, Dept Pathol & Lab Med, Sch Med, Philadelphia, PA 19104 USA

[2] Univ Miami, Miller Sch Med, Dept Microbiol & Immunol, Miami, FL 33136 USA

[3] Kings Coll London, Guys Hosp, Sch Med, Dept Immunobiol, London SE1 9RT, England

来源：

TRENDS IN IMMUNOLOGY | 2009年 / 30卷 / 07期

基金：

英国医学研究理事会;

关键词：

NECROSIS-FACTOR FAMILY; SENESCENT BALB/C MICE; INDUCED CYTIDINE DEAMINASE; HEMATOPOIETIC STEM-CELLS; TRANSCRIPTION FACTOR E47; SURROGATE LIGHT-CHAINS; AGE-RELATED DEFECTS; IG CLASS SWITCH; IMMUNE-SYSTEM; PNEUMOCOCCAL POLYSACCHARIDE-4;

D O I：

10.1016/j.it.2009.04.005

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Recent advances allow aging-associated changes in B-cell function to be approached at a mechanistic level. Reduced expression of genes crucial to lineage commitment and differentiation yield diminished B-cell production. Moreover, intrinsic differences in the repertoire generated by B-cell precursors in aged individuals, coupled with failing B-cell generation rates and life-long homeostatic competition, result in narrowed clonotypic diversity. Similarly, reductions in gene products crucial for immunoglobulin class switch recombination and somatic hypermutation impact the efficacy of humoral immune responses. Together, these findings set the stage for integrated analyses of how age-related changes at the molecular, cellular and population levels interact to yield the overall aging phenotype.

引用

页码：313 / 318

页数：6

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