Genetic basis of abnormal B cell development
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 δ5/14.1 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'.
differentiation in familial IgA deficiency and common variable immunodeficiency. Mutations
in Bruton's tyrosine kinase, immunoglobulin heavy chain and δ5/14.1 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'.
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 δ5/14.1 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’.
Elsevier