Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Editor

Personal info

View

About

Terms

Javascript disabled

Please enable Javascript support in your browser to use this application.

Instructions on how to enable JavaScript on different browsers can be found here: http://www.google.com/support/bin/answer.py?answer=23852.

[edit this page]

Coyle, A.J. et al.

Coyle, Lloyd, Tian, Nguyen, Erikkson, Wang, Ottoson, Persson, Delaney, Lehar, Lin, Poisson, Meisel, Kamradt, Bjerke, Levinson, Gutierrez-Ramos,

Crucial role of the interleukin 1 receptor family member T1/ ST2 in T helper cell type 2-mediated lung mucosal immune responses.

T1/ ST2 is an orphan receptor of unknown function that is expressed on the surface of murine T helper cell type 2 (Th2), but not Th1 effector cells. In vitro blockade of T1/ ST2 signaling with an immunoglobulin (Ig) fusion protein suppresses both differentiation to and activation of Th2, but not Th1 effector populations. In a nascent Th2-dominated response, anti-T1/ ST2 monoclonal antibody (mAb) inhibited eosinophil infiltration, interleukin 5 secretion, and IgE production. To determine if these effects were mediated by a direct effect on Th2 cells, we next used a murine adoptive transfer model of Th1- and Th2-mediated lung mucosal immune responses. Administration of either T1/ ST2 mAb or T1/ST2-Ig abrogated Th2 cytokine production in vivo and the induction of an eosinophilic inflammatory response, but failed to modify Th1-mediated inflammation. Taken together, our data demonstrate an important role of T1/ ST2 in Th2- mediated inflammatory responses and suggest that T1/ ST2 may prove to be a novel target for the selective suppression of Th2 immune responses.[1]

References

Crucial role of the interleukin 1 receptor family member T1/ST2 in T helper cell type 2-mediated lung mucosal immune responses. Coyle, A.J., Lloyd, C., Tian, J., Nguyen, T., Erikkson, C., Wang, L., Ottoson, P., Persson, P., Delaney, T., Lehar, S., Lin, S., Poisson, L., Meisel, C., Kamradt, T., Bjerke, T., Levinson, D., Gutierrez-Ramos, J.C. J. Exp. Med. (1999) [Pubmed]

Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenes Open Access Licence Privacy Policy Terms of Use apsburg

The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.