Genetic basis of abnormal B cell development

被引：62

作者：

Conley, ME

Cooper, MD

机构：

[1] Univ Alabama, Dept Med, Birmingham, AL 35294 USA

[2] Univ Alabama, Dept Pediat, Birmingham, AL 35294 USA

[3] Univ Alabama, Dept Pathol & Microbiol, Birmingham, AL 35294 USA

[4] Howard Hughes Med Inst, Birmingham, AL 35294 USA

[5] Univ Tennessee, Sch Med, Dept Pediat, Dept Immunol,St Jude Childrens Res Hosp, Memphis, TN 38105 USA

来源：

CURRENT OPINION IN IMMUNOLOGY | 1998年 / 10卷 / 04期

关键词：

D O I：

10.1016/S0952-7915(98)80112-X

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

A susceptibility gene in the MHC class III region may underlie the defective B-cell differentiation in familial IgA deficiency and common variable immunodeficiency. Mutations in Bruton's tyrosine kinase, immunoglobulin heavy chain and lambda 5/14,1 surrogate light chain loci disrupt B-cell development to cause profound antibody deficiency Mutational, biochemical and transgenic studies offer insight into the function of these and other 'antibody deficiency genes'.

引用

页码：399 / 406

页数：8

共 76 条

[71] Phosphorylation of two regulatory tyrosine residues in the activation of Bruton's tyrosine kinase via alternative receptors [J].