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Background CC 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.Methods Cells 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.Results There 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.Conclusion IL-2 and IL-4 together induced expression of CCR3 on GC B cells, and the receptor acted as a death receptor.
Background CC 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 center (GC) B cells. Methods Cells isolated from human tonsils were stimulated with IL-2 or / and IL-4 followed by bonding with eotaxin / CCL11. 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 analyze the CCR3 mRNA expressed in the GC B cells. Chemotaxis and adhesion assays were used CCL3 expression on human freshly isolated GC B cells. The combination IL-2 and IL-4 could upregulate the CCR3 mRNA and protein expression on GC B cells. Eotaxin co uld not induce GC B cell chemotaxis and adhesion but triggered apoptosis of GC B cells. Confluence IL-2 and IL-4 together induced expression of CCR3 on GC B cells, and the receptor acted as a death receptor.