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Shb deficient mice display an augmented TH2 response in peripheral CD4+ T cells

Karin Gustafsson1, Gabriela Calounova1, Fredrik Hjelm2, Vitezslav Kriz3, Birgitta Heyman4, Kjell-Olov Grönvik5, Gustavo Mostoslavsky6 and Michael Welsh1*

Author Affiliations

1 Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden

2 Olink Bioscience, Uppsala, Sweden

3 Institute of Biophysics, Academy of Science of the Czech Republic, Brno, Czech Republic

4 Department of Medical Biochemistry and Microbiology, Uppsala University, Uppsala, Sweden

5 National Veterinary Institute, Uppsala, Sweden

6 Department of Medicine, Section of Gastroenterology, and Center for Regenerative Medicine (CReM), Boston University School of Medicine, Boston, MA, USA

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BMC Immunology 2011, 12:3  doi:10.1186/1471-2172-12-3

Published: 11 January 2011



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.


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.


Our results indicate that Shb appears to play an important modulating role on TCR signaling, thus regulating the peripheral CD4+ TH2 cell response.