Download Advances in Immunology, Vol. 105 by Frederick W. Alt PDF

By Frederick W. Alt

ISBN-10: 0123813026

ISBN-13: 9780123813022

Advances in Immunology, a usual and hugely revered booklet, provides present advancements in addition to accomplished reports in immunology. Articles tackle the big variety of issues that contain immunology, together with molecular and mobile activation mechanisms, phylogeny and molecular evolution, and medical modalities. Edited and authored by means of the main scientists within the box, every one quantity offers updated details and instructions for destiny * Contributions from major gurus and specialists * Informs and updates on the entire most modern advancements within the box

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In the catabolism of globosides, a-Gal-A functions downstream of Hex-B to produce LacCer from Gb3 (Fig. 1). , 1997). 3) configuration. 3)-branched galactose could represent a physiological substrate for a-Gal-A. Consequently, enzyme deficiency in a-Gal-A activity could lead to iGb3 accumulation. , 2004b). In contrast to Hexb / mice, this deficit was only partial and specific for iNKT cells located in The Immunological Functions of Saposins 45 peripheral organs. Since Fabry and Sandhoff diseases have different etiologies and display diverse patterns of GSL storage, a generalized defect of iNKT cell selection has been proposed in LSD mice.

In addition, lysosomes are equipped with sphingolipid activator proteins (SAPs) that belong to the large and divergent family of saposin-like proteins (SAPLIPs). SAPLIP domains have been identified in relatively small proteins of about 80 amino acids in length, including the lung surfactant-associated protein B (SP-B), the tumorolytic proteins NK-lysin and granulysin, cytolytic proteins from amoeba, and several plant aspartic proteases. SAPs comprise the five molecules saposins A–D and the GM2 activator protein.

By testing the potential antigenicity of several GSL species belonging to the globo-, isoglobo-, and neolacto-series, which are produced in lysosomes upon the action of hexosaminidases (Fig. , 2004b). Hence, by removing the terminal N-acetyl-b-D-galactosamine residue from iGb4, Hex-B produces iGb3 that is recognized by iNKT cells. Possibly due to missing self on CD1d molecules, either by lack of generation (Hexb / ) or by deficient CD1d loading (pSAP / ) of endogenous antigens, both knock-out strains fail to develop iNKT cells.

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