Apoptosis in human germinal centre B cells by means of CC chemokine receptor 3 expression induced by interleukin-2 and interleukin-4 / 中华医学杂志(英文版)
Chinese Medical Journal
; (24): 665-670, 2005.
Article
in En
| WPRIM
| ID: wpr-250865
Responsible library:
WPRO
ABSTRACT
<p><b>BACKGROUND</b>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.</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>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.</p><p><b>CONCLUSION</b>IL-2 and IL-4 together induced expression of CCR3 on GC B cells, and the receptor acted as a death receptor.</p>
Full text:
1
Index:
WPRIM
Main subject:
Pathology
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Pharmacology
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RNA, Messenger
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B-Lymphocytes
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Cell Adhesion
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Chemotaxis, Leukocyte
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Interleukin-4
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Interleukin-2
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Apoptosis
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Germinal Center
Limits:
Humans
Language:
En
Journal:
Chinese Medical Journal
Year:
2005
Type:
Article