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EphB6-null mutation results in compromised T cell function.

http://www.ncbi.nlm.nih.gov/pubmed/15599401

So far, there is very limited knowledge about the role of Eph kinases, the largest family of receptor tyrosine kinases, in the immune system. Here, using EphB6(-/-) mice, we demonstrated that in vitro and in vivo T cell responses such as lymphokine secretion, proliferation, and the development of delayed-type skin hypersensitivity and experimental autoimmune encephalitis in EphB6(-/-) mice were compromised. On the other hand, humoral immune responses, such as serum levels of different Ig isotypes and IgG response to tetanus toxoid, were normal in these mice. Mechanistically, we showed that EphB6 migrated to the aggregated TCRs and rafts after TCR activation. Further downstream, in the absence of EphB6, ZAP-70 activation, LAT phosphorylation, the association of PLCgamma1 with SLP-76, and p44/42 MAPK activation were diminished. Thus, we have shown that EphB6 is pivotal in T cell function.

Pubmed ID: 15599401 RIS Download

Mesh terms: Animals | Antigens | Antigens, CD | Antigens, CD28 | Antigens, CD3 | Antigens, Differentiation, T-Lymphocyte | Biotinylation | Cell Proliferation | Cytokines | Dose-Response Relationship, Drug | Exons | Female | Flow Cytometry | Gene Deletion | Green Fluorescent Proteins | Immunoglobulin Class Switching | Lectins, C-Type | Leukocytes | Ligands | Lymphocytes | Mice | Mice, Knockout | Mice, Transgenic | Microscopy, Confocal | Models, Genetic | Mutation | Polymerase Chain Reaction | Receptor, EphB6 | Receptors, Antigen, T-Cell | Receptors, Interleukin-2 | Signal Transduction | Spleen | T-Lymphocytes | Thymus Gland | Time Factors

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