Shb Deficient Mice Display an Augmented TH2 Response in Peripheral CD4+ T Cells
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Citation (published version)Gustafsson, Karin, Gabriela Calounova, Fredrik Hjelm, Vitezslav Kriz, Birgitta Heyman, Kjell-Olov Grönvik, Gustavo Mostoslavsky, Michael Welsh. "Shb deficient mice display an augmented TH2 response in peripheral CD4+ T cells." BMC Immunology 12:3. (2011)
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+ TH cells resulting in an increased proliferative response to TCR stimulation and an elevated IL-4 production of naïve TH cells. This suggests a TH2 skewing of the Shb knockout immune system, seemingly caused by an altered TCR signaling pattern. CONCLUSION: Our results indicate that Shb appears to play an important modulating role on TCR signaling, thus regulating the peripheral CD4+ TH2 cell response.
RightsCopyright 2011 Gustafsson et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.