Premium
Fluorescence tagging and inducible depletion of PD‐L2–expressing B‐1 B cells in vivo
Author(s) -
Lee Rebecca A.,
Mao Changchuin,
Vo Hung,
Gao Wenda,
Zhong Xuemei
Publication year - 2015
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/nyas.12865
Subject(s) - phosphorylcholine , b 1 cell , cd40 , microbiology and biotechnology , biology , in vivo , immune system , antibody , naive b cell , b cell , peritoneal cavity , chemistry , antigen presenting cell , in vitro , immunology , t cell , cytotoxic t cell , biochemistry , anatomy
L2pB1 cells are a subpopulation of B‐1a B cells that express programmed death ligand 2 (PD‐L2) as their unique cell surface marker. In mice, about 50% of peritoneal B‐1a cells are L2pB1 cells. The remaining B‐1a cells are L2nB1 (PD‐L2 – ) B‐1a cells. L2pB1 cells differ from L2nB1 cells in their immunoglobulin repertoire, expression of interleukin 10, and their capacity to phagocytose phosphatidylcholine. The physiological roles of L2pB1 cells have not been investigated owing to the lack of an animal model that allows for specific depletion of L2pB1 cells. Here, we report a mouse model that enables specific tracking and inducible depletion of L2pB1 cells in vivo . Our data show that depletion of L2pB1 cells significantly reduces serum anti‐phosphorylcholine (PC) IgM levels and IL‐10 expression in the peritoneal cavity. This animal model provides a tool for the study of the immune regulatory functions of L2pB1 cells in health and disease.