Interleukin 5 and B cell differentiation.
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-5Ralpha and induces the recruitment of (beta)c to IL-5Ralpha. JAK2 and JAK1 tyrosine kinases are constitutively associated with hIL-5Ralpha 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-5Ralpha 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.
Takatsu
K
K
Department of Immunology, Institute of Medical Science, University of Tokyo, Japan.
D000818:Animals; D001402:B-Lymphocytes / Q000502:physiology*; D002454:Cell Differentiation / Q000502:physiology; D006801:Humans; D015848:Interleukin-5 / Q000502:physiology*
D015848:Interleukin-5