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Article

Reduced diabetes in btk-deficient nonobese diabetic mice and restoration of diabetes with provision of an anti-insulin IgH chain transgene.

Journal of immunology (Baltimore, Md. : 1950) - 15 Nov 2009

Kendall Peggy L, Moore Daniel J, Hulbert Chrys, Hoek Kristen L, Khan Wasif N, Thomas James W

Abstract excerpt

Type 1 diabetes results from T cell-mediated destruction of insulin-producing beta cells. Although elimination of B lymphocytes has proven successful at preventing disease, modulation of B cell function as a means to prevent type 1 diabetes has not been investigated. The development, fate, and function of B lymphocytes depend upon BCR signaling, which is mediated in part by Bruton's tyrosine kinase (BTK). When...

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Share to Agammaglobulinaemia Tyrosine Kinase
Share to B-Lymphocyte Subsets

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Share to Immunoglobulin Heavy Chains

Share to Insulin Antibodies

Share to Mice, Inbred NOD

Share to Receptors, Antigen, B-Cell

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Source

Open in PubMed Open full text

Identifiers

PMID: 19841184
DOI: 10.4049/jimmunol.0900367
PMCID: PMC2970569

Genes

BCR
BTK

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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