CD1d(hi)CD5⁺ B cells differentiate into antibody-secreting cells under the stimulation with calreticulin fragment.
10.1007/s13238-013-3062-5
- Author:
Tengteng ZHANG
1
;
Yun XIA
;
Lijuan ZHANG
;
Wanrong BAO
;
Chao HONG
;
Xiao-Ming GAO
Author Information
1. Institutes of Biology and Medical Sciences, Soochow University, Suzhou, 215123, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Antigens, CD1d;
metabolism;
Autoantibodies;
biosynthesis;
B-Lymphocytes;
cytology;
drug effects;
immunology;
metabolism;
CD5 Antigens;
metabolism;
Calreticulin;
chemistry;
Cell Differentiation;
drug effects;
Encephalomyelitis, Autoimmune, Experimental;
immunology;
Humans;
Mice;
Peptide Fragments;
chemistry;
pharmacology;
Solubility
- From:
Protein & Cell
2013;4(11):872-881
- CountryChina
- Language:English
-
Abstract:
Calreticulin (CRT) is a multifunctional molecule in both intracellular and extracellular environment. We have previously found that a recombinant CRT fragment (rCRT/39-272) could modulate T cell-mediated immunity in mice via activation and expansion of CD1d(hi)CD5⁺ B cells as well as induction of CRT-specific regulatory antibodies. Antibody secreting cells (ASCs) are terminally differentiated B cells responsible for producing antibodies to participate in positive immune response as well as immune regulation. In this study, we demonstrate that rCRT/39-272 differentiates murine CD1d(hi)CD5⁺ B cells into ASCs marked by increased expression of plasma cell-associated transcription factors and production of polyreactive antibodies against DNA and CRT in vitro. Intraperitoneal administration of rCRT/39-272 augmented differentiation of CD1d(hi)CD5⁺ B cells into ASCs in naïve mice or mice with experimental autoimmune encephalomyelitis. Thus, we propose that ASC differentiation and subsequent antibody production of CD1d(hi)CD5⁺ B cells are key steps in CRT-mediated immunoregulation on inflammatory T cell responses.
