New PDF release: Annual Review of Immunology Volume 26 2008

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Extra resources for Annual Review of Immunology Volume 26 2008

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In contrast, in T1D, there is no significant correlation between the T allele and the appearance or levels of autoantibodies. Also, the role of LYP in the autoantibody response may not necessarily be intrinsic to B cells but rather a consequence of altered T cell help. The uncertainty regarding which cells are phenotypically affected by LYP∗ W620 in different disease settings is further exemplified by a recent study demonstrating that carriers of the T1858 allele are more prone to certain infectious diseases, such as invasive pneumococcal infections and Gram-positive empyema (79).

All PEST group PTPs can normally through their CTH domain bind the coiled-coil domain of CD2BP1/PSTPIP (19) (T. V. Miletic & T. Mustelin, unpublished data), but the disease-associated mutated form of CD2BP1 exhibits more than 90% reduction in its ability to interact with PTP-PEST (88). Most likely, the binding between disease-associated CD2BP1 and LYP/PTP-HSCF is affected Annu. Rev. Immunol. 26:29-55. org by Shanghai Information Center for Life Sciences on 04/28/08. For personal use only. PTK: protein tyrosine kinase 40 Vang et al.

V. Miletic & T. Mustelin, unpublished observations). Mice deficient in PEP have normal resting T cell numbers and subpopulations but exhibit enhanced memory T cell responses (33). Furthermore, restimulation of T cells from these animals is associated with elevated and sustained TCR-induced phosphorylation of both Lck-Y394 and of ZAP-70, as well as augmented proliferation. The lack of a noticeable phenotype in naive T cells from PEP−/− mice may be due to redundancy with PTP-PEST (Y. Arimura & T. Mustelin, unpublished observations).

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