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PubMed · 4623402

Quantitative method for determining human G allotype antigens (Gm). II. Differences in Gm gene expression for G1 and G3 H chains in sera.

S D Litwin·S Balaban
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AgammaglobulinemiaAllelesAutoanalysisBlood Group AntigensGenesHemagglutination Inhibition TestsHeterozygoteHomozygoteHumansHypergammaglobulinemiaImmunodiffusionImmunoglobulin GImmunoglobulinsIsoantigensMultiple MyelomaPhenotypeWhite PeopleJournal Article

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S D Litwin, S Balaban. 1972. Quantitative method for determining human G allotype antigens (Gm). II. Differences in Gm gene expression for G1 and G3 H chains in sera.. https://pubmed.ncbi.nlm.nih.gov/4623402/

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The critical role of Bruton tyrosine kinase (Btk) in B cells has been documented by the block of B-cell development in X-linked agammaglobulinemia (XLA). Less is known about Btk function in myeloid cells. Several pieces of evidence indicate that Btk is a component of Toll-like receptor (TLR) signaling. We analyzed whether Btk deficiency in XLA is associated with an impaired dendritic cell (DC) compartment or defective TLR signaling. We analyzed the expression of TLRs 1 to 9 on myeloid DCs generated from XLA patients and evaluated their response to activation by specific TLR agonists. We show that XLA patients have normal numbers of circulating DCs. Btk-deficient DCs have no defect in response to stimulation of TLRs 1/2, 2/6, 3, 4, and 5 but display a profound impairment of IL-6 and TNF-alpha production in response to stimulation by TLR-8 cognate agonist, ssRNA. These findings may provide an explanation for the susceptibility to enteroviral infections in XLA patients.

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