Loading…
The inhibitory receptor CD300a is up‐regulated by hypoxia and GM‐CSF in human peripheral blood eosinophils
Background Eosinophils are involved in several inflammatory processes including allergic inflammation. It has been shown that eosinophil functions may be regulated by activating or inhibitory receptors. Hypoxia is a feature of inflamed tissues and has recently been shown to regulate eosinophil viabi...
Saved in:
Published in: | Allergy (Copenhagen) 2013-03, Vol.68 (3), p.397-401 |
---|---|
Main Authors: | , , , |
Format: | Article |
Language: | English |
Subjects: | |
Online Access: | Get full text |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
Summary: | Background
Eosinophils are involved in several inflammatory processes including allergic inflammation. It has been shown that eosinophil functions may be regulated by activating or inhibitory receptors. Hypoxia is a feature of inflamed tissues and has recently been shown to regulate eosinophil viability and pro‐angiogenic potential. In this study, the effect of hypoxia and GM‐CSF on the inhibitory receptor CD300a in human peripheral blood eosinophils was investigated.
Methods
CD300a expression on eosinophils was analyzed by flow cytometry and evaluated by immuno‐fluorescence; mRNA levels were evaluated by RT‐PCR.
Results
An increase in the expression of CD300a was observed in hypoxic eosinophils compared to the normoxic ones. GM‐CSF strongly induced CD300a increase also after 3 h in culture. In addition, hypoxia augmented mRNA levels of CD300a. Inhibition of hypoxia‐inducible factor (HIF)‐1 abolished the hypoxia‐/GM‐CSF‐induced CD300a increase.
Conclusion
CD300a expression is up‐regulated by hypoxia, and GM‐CSF where HIF‐1 might play an important role. These results are important for the understanding of eosinophils behavior in inflamed tissue and suggest a new effect on their function in allergic inflammation. Taken together our data point out CD300a as a novel target for the treatment of allergy. |
---|---|
ISSN: | 0105-4538 1398-9995 |
DOI: | 10.1111/all.12092 |