NDLI: Bruton's tyrosine kinase promotes persistence of mature anti-insulin B cells.

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Bruton's tyrosine kinase promotes persistence of mature anti-insulin B cells.

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Bruton's tyrosine kinase promotes persistence of mature anti-insulin B cells.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Hoek, Kristen L. Sullivan, Allison M. Case, James B. Bonami, Rachel H. Khan, Wasif N. Kendall, Peggy L. Steinberg, Hannah E.
Description	Author Affiliation: Bonami RH ( Division of Rheumatology and Immunology, Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN 37232)
Abstract	Autoreactive B lymphocytes are essential for the development of T cell-mediated type 1 diabetes (T1D). Cytoplasmic Bruton's tyrosine kinase (BTK) is a key component of B cell signaling, and its deletion in T1D-prone NOD mice significantly reduces diabetes. However, the role of BTK in the survival and function of autoreactive B cells is not clear. To evaluate the contributions of BTK, we used mice in which B cells express an anti-insulin BCR (125Tg) and promote T1D, despite being anergic. Crossing Btk deficiency onto 125Tg mice reveals that, in contrast to immature B cells, mature anti-insulin B cells are exquisitely dependent upon BTK, because their numbers are reduced by 95%. BTK kinase domain inhibition reproduces this effect in mature anti-insulin B cells, with less impact at transitional stages. The increased dependence of anti-insulin B cells on BTK became particularly evident in an Igκ locus site-directed model, in which 50% of B cells edit their BCRs to noninsulin specificities; Btk deficiency preferentially depletes insulin binders from the follicular and marginal zone B cell subsets. The persistent few Btk-deficient anti-insulin B cells remain competent to internalize Ag and invade pancreatic islets. As such, loss of BTK does not significantly reduce diabetes incidence in 125Tg/NOD mice as it does in NOD mice with a normal B cell repertoire. Thus, BTK targeting may not impair autoreactive anti-insulin B cell function, yet it may provide protection in an endogenous repertoire by decreasing the relative availability of mature autoreactive B cells.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1300125
Journal	The Journal of Immunology
Issue Number	4
Volume Number	192
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2014-02-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Insulin Antibodies Immunology Insulin Protein-tyrosine Kinases Animals B-lymphocytes Cells, Cultured Diabetes Mellitus, Type 1 Immunoglobulins Mice Mice, Inbred C57bl Mice, Inbred Nod Mice, Transgenic Genetics Receptors, Antigen, B-cell Metabolism Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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