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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Di, Caixia Liu, Junling Yuan, Yufan Zhou, Tong Xia, Zhenwei Zhong, Wenwei Lin, Xiaoliang Zhang, Yanjie |
| Description | Author Affiliation: Di C ( From the Department of Pediatrics, Ruijin Hospital affiliated with Shanghai Jiao Tong University School of Medicine, 197 Ruijin 2nd Road, Shanghai 200025, China.); Lin X ( From the Department of Pediatrics, Ruijin Hospital affiliated with Shanghai Jiao Tong University School of Medicine, 197 Ruijin 2nd Road, Shanghai 200025, China.); Zhang Y ( From the Department of Pediatrics, Ruijin Hospital affiliated with Shanghai Jiao Tong University School of Medicine, 197 Ruijin 2nd Road, Shanghai 200025, China.); Zhong W ( Department of Pediatrics, Shanghai Children's Medical Center affiliated with Shanghai Jiao Tong University School of Medicine, 1678 Dongfang Road, Shanghai 200127, China, and.); Yuan Y ( From the Department of Pediatrics, Ruijin Hospital affiliated with Shanghai Jiao Tong University School of Medicine, 197 Ruijin 2nd Road, Shanghai 200025, China.); Zhou T ( From the Department of Pediatrics, Ruijin Hospital affiliated with Shanghai Jiao Tong University School of Medicine, 197 Ruijin 2nd Road, Shanghai 200025, China.); Liu J ( Department of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory of Tumor Microenvironment and Inflammation, Shanghai Jiao Tong University School of Medicine, 280 South Chongqing Road, Shanghai 200025, China.); Xia Z ( From the Department of Pediatrics, Ruijin Hospital affiliated with Shanghai Jiao Tong University School of Medicine, 197 Ruijin 2nd Road, Shanghai 200025, China, xzw63@hotmail.com.) |
| Abstract | Asthma is characterized by increased airway submucosal infiltration of T helper (Th) cells and myeloid cells that co-conspire to sustain a chronic inflammation. While recent studies have demonstrated that the myeloid basophils promote Th2 cells in response to various types of allergens, the underlying mechanisms are poorly understood. Here, we found for the first time that in a mouse model of allergic asthma basophils highly expressed OX40 ligand (OX40L) after activation. Interestingly, blockade of OX40-OX40L interaction suppressed basophils-primed Th2 cell differentiation in vitro and ameliorated ovalbumin (OVA)-induced allergic eosinophilic inflammation mediated by Th2 activation. In accordance, the adoptive transfer of basophils derived from mediastinal lymph nodes (MLN) of OVA-immunized mice triggered a robust Th2 response and eosinophilic inflammation in wild-type mice but largely muted in OX40(-/-) mice and mice receiving OX40L-blocked basophils. Taken together, our results reveal a critical role of OX40L presented by the activated basophils to initiate Th2 responses in an allergic asthma model, implicating OX40-OX40L signaling as a potential therapeutic target in the treatment of allergic airway inflammation. |
| ISSN | 00219258 |
| e-ISSN | 1083351X |
| Journal | Journal of Biological Chemistry |
| Issue Number | 20 |
| Volume Number | 290 |
| Language | English |
| Publisher | American Society for Biochemistry and Molecular Biology (United States) |
| Publisher Date | 2015-05-15 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Asthma Immunology Basophils Gene Expression Regulation Membrane Glycoproteins Th2 Cells Tumor Necrosis Factors Animals Genetics Pathology Therapy Disease Models, Animal Mice Mice, Knockout Research Support, Non-U.S. Gov't Biochemistry Molecular Biology |
| Content Type | Text |
| Resource Type | Article |
| Subject | Cell Biology Biochemistry Molecular Biology |
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