Annual Review of Immunology Volume 26 2008 by Annual Reviews PDF

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All the members of these three classes of PTPs use a cysteine-based catalytic mechanism. In contrast, class IV PTPs are aspartate based and are currently represented by the four Eya genes. The expression patterns of individual PTPs vary from ubiquitous to strictly tissue specific. Most cells express 30% to 60% of the entire complement of PTPs. Neuronal and hematopoietic cells tend to express a relatively high number of PTPs. T cells, for instance, contain between 60 and 70 different PTPs, and a similar set is found in B cells (18).

ANRV338-IY26-02 ARI 16 February 2008 11:8 of T1D (61), a later study could not confirm this connection (62), again supporting a role for C1858T as the major T1D-associated SNP in PTPN22 (63). However, it is still possible that additional polymorphisms may be discovered for PTPN22 and that these are independently related to different and/or overlapping groups of autoimmune disorders. For instance, one recent study suggested that the C1858T SNP was not associated with psoriasis but that there was evidence for a susceptibility locus for this disease somewhere else in PTPN22 or in its vicinity (64).

1963. A biochemical abnormality in hereditary angioneurotic edema: absence of serum inhibitor of C’1-esterase. Am. J. Med. 35:37–44 117. Austen KF, Sheffer AL. 1965. Detection of hereditary angioneurotic edema by demonstration of a profound reduction in the second component of human complement. N. Engl. J. Med. 272:649–56 118. Ruddy S, Austen KF. 1967. A stoichiometric assay for the fourth component of complement in whole human serum using EAC’1agp and functionally pure human second component. J.

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Annual Review of Immunology Volume 26 2008 by Annual Reviews

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