0440859 - BFÚ 2015 RIV GB eng J - Článek v odborném periodiku
Gustafsson, K. - Calounova, G. - Hjelm, F. - Kříž, Vitězslav - Heyman, B. - Gronvik, K.O. - Mostoslavsky, G. - Welsh, M.
Shb deficient mice display an augmented T(H)2 response in peripheral CD4+T cells.
BMC Immunology. Roč. 12, č. 3 (2011). ISSN 1471-2172. E-ISSN 1471-2172
Institucionální podpora: RVO:68081707
Klíčová slova: DOMAIN PROTEIN SHB * JURKAT T-CELLS * ANTIGEN RECEPTOR
Kód oboru RIV: BO - Biofyzika
Impakt faktor: 2.531, rok: 2011
DOI: https://doi.org/10.1186/1471-2172-12-3

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.
Trvalý link: http://hdl.handle.net/11104/0243967