[Sign in] [Register]   

EIAab logo

EIAab news detail, please contact if you have any questions about online orders and payment.
Interleukin-13 interferes with activation-induced t-cell apoptosis by repressing p53 expression
Update time:2016-09-07 01:25:57   【 Font: Large  Medium Small


The etiology and the underlying mechanism of CD4+ T-cell polarization are unclear. This study sought to investigate the mechanism by which interleukin (IL)-13 prevents the activation-induced apoptosis of CD4+ T cells. Here we report that CD4+ T cells expressed IL-13 receptor α2 in the intestine of sensitized mice. IL-13 suppressed both the activation-induced apoptosis of CD4+ T cells and the expression of p53 and FasL. Exposure to recombinant IL-13 inhibited activation-induced cell death (AICD) along with the expression of p53, caspase 3, and tumor necrosis factor-α in CD4+ T cells. Administration of an anti-IL-13 antibody enhanced the effect of specific immunotherapy on allergic inflammation in the mouse intestine, enforced the expression of p53 in intestinal CD4+ T cells, and enhanced the frequency of CD4+ T-cell apoptosis upon challenge with specific antigens. In summary, blocking IL-13 enhances the therapeutic effect of antigen-specific immunotherapy by regulating apoptosis and thereby enforcing AICD in CD4+ T cells.

Cited products
Source:Cellular & molecular immunology      by Yang L, Xu L Z, Liu Z Q, et al.
Hot Genes
ALCAM ACE KSR2 ASPRO C19orf80 Gdf5 Trap1a Atf2
Top Searches
Ubiquitin ELISA Ubiquitin-protein ligase metalloproteinase Asprosin Tumor necrosis TRAP1A vitamin d
Why choose EIAAB
Our products have been quoted by many publications in famous journals such as Cell; Cell Metabolism; Hepatology; Biomaterials.more
Further Information
About us Protein center Bank account Distributors Terms & Conditions Career

Copyright & copy www.eiaab.com2006-2016 All Rights Reserved    EIAab