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B Cell-Specific Deficiency for Smad2 In Vivo Leads to Defects in TGF-β-Directed IgA Switching and Changes in B Cell Fate

1 Feb 2006

Abstract excerpt

Smad2 is a member of the intracellular mediators that transduce signals from TGF-beta receptors and activin receptors. Targeted inactivation of Smad2 in mice leads to early lethality before gastrulation. It was shown previously that TGF-betaRII deficiency in vivo leads to defects in B cell homeostasis, Ag responsiveness, and IgA class switch recombination of B cells. To investigate the importance of...

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PMID: 16455997
DOI: 10.4049/jimmunol.176.4.2389

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