Show simple item record

dc.contributor.authorGustafsson, Karinen_US
dc.contributor.authorCalounova, Gabrielaen_US
dc.contributor.authorHjelm, Fredriken_US
dc.contributor.authorKriz, Vitezslaven_US
dc.contributor.authorHeyman, Birgittaen_US
dc.contributor.authorGrönvik, Kjell-Oloven_US
dc.contributor.authorMostoslavsky, Gustavoen_US
dc.contributor.authorWelsh, Michaelen_US
dc.date.accessioned2011-12-29T21:01:36Z
dc.date.available2011-12-29T21:01:36Z
dc.date.copyright2011en_US
dc.date.issued2011-1-11en_US
dc.identifier.citationGustafsson, 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)en_US
dc.identifier.issn1471-2172en_US
dc.identifier.urihttps://hdl.handle.net/2144/2493
dc.description.abstractBACKGROUND: 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.en_US
dc.description.sponsorshipThe Swedish Research Council; Swedish Cancer Foundation; Swedish Diabetes Association; Uppsala University, Sweden; Wallenberg Foundation; Family Ernfors Fund; Anna Maria Lundin Stipendfund; Sederholm Funden_US
dc.language.isoenen_US
dc.publisherBioMed Central>en_US
dc.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.en_US
dc.rights.urihttp://creativecommons.org/licenses/by/2.0en_US
dc.titleShb Deficient Mice Display an Augmented TH2 Response in Peripheral CD4+ T Cellsen_US
dc.typeArticleen_US
dc.identifier.doi10.1186/1471-2172-12-3en_US
dc.identifier.pmid21223549en_US
dc.identifier.pmcid3024994en_US


This item appears in the following Collection(s)

Show simple item record

Copyright 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.
Except where otherwise noted, this item's license is described as Copyright 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.