By J. Lindsay Whitton (auth.), J. Lindsay Whitton M.D., Ph.D. (eds.)
Antigen presentation is principal to the immune reaction, andis instrumental in making sure that the reaction fastened is that most suitable to the eradication of the actual microbe confronted. during this quantity, specialists within the box offer state of the art descriptions of the antigen presentation pathways. How do viruses disrupt those severe pathways, and to what impression? Do all tissues current antigen within the related method? If now not, why? What are the results of dysfunctional antigen presentation, noticeable in convinced genetic issues? This publication considers not just the molecular info, but in addition their relevance to the full organism.
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Extra info for Antigen Presentation
1996), although this does not necessarily indicate TAP independence. Finally, CD8+ T cells isolated from TAp-/mice are still present in low but significant numbers and possess epitope-specific cytotoxic activity (ALDRICH et al. 1994b; VAN SANTEN et al. 1995; SANDBERG et al. 1996). Peptide affinity for TAP ranges from 410 to 1600 nM, with approximately 105_106 binding sites per cell (VAN ENDERT et al. 1994a; UEBEL et al. 1995; YANG and BRACIALE 1995; KOOPMAN et aI. 1996). Overexpression ofTAPI and TAP2 in insect cells has shown that these two proteins form a heterodimer capable of transporting peptides in the presence of ATP without any requirement for accessory proteins (MEYER et al.
Although the role of ubiquitination and degradation of ubiquitinated proteins by 26S proteasomes in MHC class I antigen processing is tenuous, it is clear that 20S proteasomes playa major role (see above discussion). Once generated, peptides have a remarkably short half-life in cells, but the binding to MHC class I molecules prevents their degradation and extends their half-life (MALARKANNAN et al. 1995b). 2 Peptide Size Digestion of ovalbumin-derived peptides 22-44 amino acids long with proteasomes in vitro resulted in the formation of peptides eight to 11 amino acids long (NIEDERMANN et al.
1995) but not others (HANAU et al. 1994; BRUTKIEWICZ et aI. 1995; HOLCOMBE et al. 1995). Although presentation of most MHC class I-binding peptides is dependent on TAP, some peptides may be delivered to the ER by one or more TAP-independent pathways. A subset of HLA-A2 molecules bind ER translocation signal peptides, which are already present in the ER, thereby circumventing the requirement for TAP (HENDERSON et al. 1992; WEI and CRESSWELL 1992). CTL can also be generated to some viral proteins containing ER insertion sequences (ANDERSON et al.