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PubMed · 9722915

Genetic basis of abnormal B cell development.

M E Conley·M D Cooper
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Abstract

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'.

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Agammaglobulinaemia Tyrosine KinaseAgammaglobulinemiaAnimalsB-LymphocytesCell DifferentiationCommon Variable ImmunodeficiencyHumansIgA DeficiencyImmunoglobulin Heavy ChainsImmunoglobulin Light ChainsImmunoglobulin Light Chains, SurrogateImmunoglobulin mu-ChainsMembrane GlycoproteinsMiceProtein-Tyrosine KinasesX ChromosomeJournal ArticleReview

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M E Conley, M D Cooper. 1998. Genetic basis of abnormal B cell development.. https://doi.org/10.1016/s0952-7915(98)80112-x

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Agammaglobulinaemia Tyrosine Kinase↗
PubMed2007

Btk regulates multiple stages in the development and survival of B-1 cells.

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