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Shb deficient mice display an augmented T(H)2 response in peripheral CD4+T cells
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SYSNO ASEP 0440859 Druh ASEP J - Článek v odborném periodiku Zařazení RIV J - Článek v odborném periodiku Poddruh J Článek ve WOS Název Shb deficient mice display an augmented T(H)2 response in peripheral CD4+T cells Tvůrce(i) Gustafsson, K. (SE)
Calounova, G. (SE)
Hjelm, F. (SE)
Kříž, Vitězslav (BFU-R)
Heyman, B. (US)
Gronvik, K.O. (SE)
Mostoslavsky, G. (US)
Welsh, M. (SE)Celkový počet autorů 8 Zdroj.dok. BMC Immunology. - : BMC - ISSN 1471-2172
Roč. 12, č. 3 (2011)Poč.str. 6 s. Forma vydání Online - E Jazyk dok. eng - angličtina Země vyd. GB - Velká Británie Klíč. slova DOMAIN PROTEIN SHB ; JURKAT T-CELLS ; ANTIGEN RECEPTOR Vědní obor RIV BO - Biofyzika Institucionální podpora BFU-R - RVO:68081707 UT WOS 000286477200001 DOI https://doi.org/10.1186/1471-2172-12-3 Anotace Background: Shb, a ubiquitously expressed Src homology 2 domain-containing adaptor protein has previously been implicated in the signaling of various tyrosine kinase receptors including the TCR. Shb associates with SLP76, LAT and Vav, all important components in the signaling cascade governing T cell function and development. A Shb knockout mouse was recently generated and the aim of the current study was to address the importance of Shb deficiency on T cell development and function. Results: Shb knockout mice did not display any major changes in thymocyte development despite an aberrant TCR signaling pattern, including increased basal activation and reduced stimulation-induced phosphorylation. The loss of Shb expression did however affect peripheral CD4+ T-H cells resulting in an increased proliferative response to TCR stimulation and an elevated IL-4 production of naive T-H cells. This suggests a T(H)2 skewing of the Shb knockout immune system, seemingly caused by an altered TCR signaling pattern. Pracoviště Biofyzikální ústav Kontakt Jana Poláková, polakova@ibp.cz, Tel.: 541 517 244 Rok sběru 2015
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