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Autoimmunity and inflammation due to a gain-of-function mutation in phospholipase C gamma 2 that specifically increases external Ca2+ entry.

Abstract：

:The identification of specific genetic loci that contribute to inflammatory and autoimmune diseases has proved difficult due to the contribution of multiple interacting genes, the inherent genetic heterogeneity present in human populations, and a lack of new mouse mutants. By using N-ethyl-N-nitrosourea (ENU) mutagenesis to discover new immune regulators, we identified a point mutation in the murine phospholipase Cg2 (Plcg2) gene that leads to severe spontaneous inflammation and autoimmunity. The disease is composed of an autoimmune component mediated by autoantibody immune complexes and B and T cell independent inflammation. The underlying mechanism is a gain-of-function mutation in Plcg2, which leads to hyperreactive external calcium entry in B cells and expansion of innate inflammatory cells. This mutant identifies Plcg2 as a key regulator in an autoimmune and inflammatory disease mediated by B cells and non-B, non-T haematopoietic cells and emphasizes that by distinct genetic modulation, a single point mutation can lead to a complex immunological phenotype.

journal_name

Immunity

journal_title

Immunity

authors

Yu P,Constien R,Dear N,Katan M,Hanke P,Bunney TD,Kunder S,Quintanilla-Martinez L,Huffstadt U,Schröder A,Jones NP,Peters T,Fuchs H,de Angelis MH,Nehls M,Grosse J,Wabnitz P,Meyer TP,Yasuda K,Schiemann M,Schneider-Fr

doi

10.1016/j.immuni.2005.01.018

keywords:

subject

Has Abstract

pub_date

2005-04-01 00:00:00

pages

451-65

issue

4

eissn

1074-7613

issn

1097-4180

pii

S1074-7613(05)00099-3

journal_volume

22

pub_type

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