Interleukin-2 primes eosinophil degranulation in hypereosinophilia and Wells' syndrome

被引：67

作者：

Simon, HU

Plötz, S

Simon, D

Seitzer, U

Braathen, LR

Menz, G

Straumann, A

Dummer, R

Levi-Schaffer, F

机构：

[1] Univ Bern, Dept Pharmacol, CH-3010 Bern, Switzerland

[2] Hebrew Univ Jerusalem, Hadassah Med Sch, Sch Pharm, Dept Pharmacol, IL-91010 Jerusalem, Israel

[3] Univ Zurich, Dept Dermatol, Zurich, Switzerland

[4] Kantonsspital Olten, Dept Gastroenterol, Olten, Switzerland

[5] High Altitude Clin Davos Wolfgang, Davos, Switzerland

[6] Res Ctr Borstel, Div Vet Infectiol & Immunol, Dept Cell Biol & Immunol, Borstel, Germany

[7] Univ Bern, Dept Dermatol, Bern, Switzerland

[8] Tech Univ Munich, Dept Dermatol, Div Environm Dermatol & Allergy GSF FUM, D-8000 Munich, Germany

来源：

EUROPEAN JOURNAL OF IMMUNOLOGY | 2003年 / 33卷 / 04期

关键词：

eosinophil; degranulation; IL-2; hypereosinophilia; priming;

D O I：

10.1002/eji.200323727

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Patients with hypereosinophilia frequently suffer from eosinophil-mediated damages of the heart, lungs, skin, and other organs, while some do not. The reason(s) for this difference is not known. We observed that eosinophils from most patients with hypereosinophilia express the a-chain of the IL-2 receptor (CD25), and that IL-2 enhances platelet-activating factor-stimulated release of eosinophil cationic protein from CD25-expressing but not from CD25-negative eosinophils. Such a "priming" effect has previously been described for eosinophil hematopoietins. These data suggest that patients with increased eosinophil surface CD25 expression are at higher risk of eosinophil degranulation and subsequent tissue damage when IL-2 is present at inflammatory sites.

引用

页码：834 / 839

页数：6

共 27 条

[1] WELLS SYNDROME IS A DISTINCTIVE DISEASE ENTITY AND NOT A HISTOLOGIC DIAGNOSIS [J].