Apoptosis in human germinal centre B cells by means of CC chemokine receptor 3 expression induced by interleukin-2 and interleukin-4.
- Author:
Qiu-ping ZHANG
1
;
Luo-kun XIE
;
Li-jun ZHANG
;
Jin-quan TAN
Author Information
- Publication Type:Journal Article
- MeSH: Apoptosis; B-Lymphocytes; metabolism; pathology; Cell Adhesion; Chemotaxis, Leukocyte; Germinal Center; metabolism; pathology; Humans; Interleukin-2; pharmacology; Interleukin-4; pharmacology; RNA, Messenger; analysis; Receptors, CCR3; Receptors, Chemokine; genetics
- From: Chinese Medical Journal 2005;118(8):665-670
- CountryChina
- Language:English
-
Abstract:
BACKGROUNDCC chemokine receptor 3 (CCR3), expressed on some inflammatory cells, is a member of the chemokine receptor family. Its ligand is eotaxin/CCL11. In this research, we studied the expression and function of CCR3 induced by interleukin-2 (IL-2) and interleukin-4 (IL-4) on human germinal centre (GC) B cells.
METHODSCells isolated from human tonsils were stimulated with IL-2 or/and IL-4 followed by bonding with eotaxin/CCL11. Flow cytometry was used to detect expression of CCR3 on GC B cells and apoptosis of GC B cells. Real time quantitative reverse transcription polymerase chain reaction and Northern blot assays were used to analyse the CCR3 mRNA expressed in the GC B cells. Chemotaxis and adhesion assays were used to determine the effect of eotaxin/CCL11 ligand bonded to CCR3 on GC B cells.
RESULTSThere was no CCR3 expression on human freshly isolated GC B cells. The combination IL-2 and IL-4 could upregulate CCR3 mRNA and protein expression on GC B cells. Eotaxin could not induce GC B cell chemotaxis and adhesion but triggered apoptosis of GC B cells.
CONCLUSIONIL-2 and IL-4 together induced expression of CCR3 on GC B cells, and the receptor acted as a death receptor.
