Interleukin 5 and B cell differentiation

被引：63

作者：

Takatsu, K ^{[1
]}

机构：

[1] Univ Tokyo, Inst Med Sci, Dept Immunol, Minato Ku, Tokyo 108, Japan

来源：

CYTOKINE & GROWTH FACTOR REVIEWS | 1998年 / 9卷 / 01期

关键词：

B-l cells; IgA production; Ig isotope switching; eosinophil; BtK;

D O I：

10.1016/S1359-6101(97)00034-8

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Interleukin-5 (IL-5) stimulates proliferation and differentiation of B cells and eosinophils. IL-5 receptor (IL-5R) comprises alpha and beta c chains. IL-5 specifically binds to IL-5R alpha and induces the recruitment of beta c to IL-5R alpha. JAK2 and JAK1 tyrosine kinases are constitutively associated with hIL-5R alpha and beta c, respectively and activated upon IL-5 stimulation. IL-5 induces tyrosine phosphorylations of cellular proteins including beta c and STAT5 and activates Btk. X-linked immunodeficient mice have B-cell-specific defects due to missense mutation of the btk gene. The cytoplasmic proline-rich regions of both IL-5R alpha and beta c are essential for the IL-5 signalling. IL-5 appears to play a critical role in hypereosinophilic syndromes and atopic diseases. The treatment of animals with anti-IL-5 mAb can decrease the enhanced bronchial responsiveness induced by allergen sensitization. Clinical studies provide a strong impetus for investigating the means of modulating IL-5 effects. (C) 1998 Elsevier Science Ltd. All rights reserved.

引用

页码：25 / 35

页数：11

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