Point mutations in the gene encoding IP3 receptor subtype 3 cause impairment in T-cell and B-cell immune responses via dysfunctional Ca2+ mobilization

摘要

In the current issue of this journal,Neumann et al.provide novel insights into the role of inositol-1,4,5-trisphosphate receptor subtype 3(IP3R3)in combined immunodeficiency[1].They show that subjects with heterozygous variants in IP3R3 have dysfunctional Ca2+mobilization from the endoplasmic reticulum and impaired proliferation of T and B cells.These observations demonstrate that adaptive immune cells such as T and B cells are prone to defects in IP3R3-Ca2+signaling.This highlights a new dimension to the function of IP3R3 in adaptive immune cells that was hitherto unknown.