| Summary: | <p>Abstract</p> <p>Background</p> <p>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 <it>Shb </it>knockout mouse was recently generated and the aim of the current study was to address the importance of <it>Shb </it>deficiency on T cell development and function.</p> <p>Results</p> <p><it>Shb </it>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<sub>H </sub>cells resulting in an increased proliferative response to TCR stimulation and an elevated IL-4 production of naïve T<sub>H </sub>cells. This suggests a T<sub>H</sub>2 skewing of the <it>Shb </it>knockout immune system, seemingly caused by an altered TCR signaling pattern.</p> <p>Conclusion</p> <p>Our results indicate that Shb appears to play an important modulating role on TCR signaling, thus regulating the peripheral CD4+ T<sub>H</sub>2 cell response.</p>
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