Recognition of Double-Stranded RNA by TLR3 Induces Severe Small Intestinal Injury in Mice | Zendy

Rongbin Zhou | Zendy; Haiming Wei | Zendy; Rui Sun | Zendy; Zhigang Tian | Zendy

AI Assistant Blog Pricing

Home ZAIA Blog

Open Access

Recognition of Double-Stranded RNA by TLR3 Induces Severe Small Intestinal Injury in Mice

Author(s) -

Rongbin Zhou,

Haiming Wei,

Rui Sun,

Zhigang Tian

Publication year - 2007

Publication title -

the journal of immunology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.737

H-Index - 372

eISSN - 1550-6606

pISSN - 0022-1767

DOI - 10.4049/jimmunol.178.7.4548

Subject(s) - tlr3 , intraepithelial lymphocyte , rna silencing , cd8 , cd3 , biology , pathogenesis , rotavirus , gene silencing , homeostasis , immunology , microbiology and biotechnology , rna , immune system , innate immune system , gene , rna interference , toll like receptor , virus , genetics

The role of TLRs on intestinal epithelial cells (IECs) is controversial, and the mechanisms by which TLRs influence mucosal homeostasis are obscure. In this study, we report that genomic dsRNA from rotavirus, and its synthetic analog polyinosinic-polycytidylic acid (poly(I:C)), induce severe mucosal injury in the small intestine. Upon engaging TLR3 on IECs, dsRNA triggers IECs to secrete IL-15, which functions to increase the percentage of CD3+NK1.1+ intestinal intraepithelial lymphocytes (IELs) and enhances the cytotoxicity of IELs. Moreover, The CD3+NK1.1+ IELs are proved as CD8alphaalpha+ IELs. These results provide direct evidence that abnormal TLR3 signaling contributes to breaking down mucosal homeostasis and the first evidence of pathogenic effects mediated by CD8alphaalpha+ IELs. The data also suggest that genomic dsRNA may be involved in the pathogenesis of acute rotavirus gastroenteritis.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.

Having issues? You can contact us here

Accelerating Research