Epitopes mechanisms

To better understand the critical role of oligosaccharide-receptor interactions and their molecular mechanisms through the cluster-effect, and thus access optimized synthetic ligands, several research groups have shown creativity in proposing original multivalent platforms that could allow for tailored valencies, dimensions, and epitope orientations. 

The mechanism most commonly invoked to explain the association of infection with autoimmune disease is molecular mimicry that is, the concept that antigens (or more properly, epitopes) of the microorganism closely resemble self-antigens.50 The induction of an immune response to the microbial antigen thus results in cross-reactivity with selfantigens and the induction of autoimmunity. Although epitope specific cross-reactivity has been shown in some animal models,48,51 53 molecular mimicry is clearly demonstrated to be the causative mechanism in few, if any, human diseases.3 54,55... 

There is considerable interest in the role of infectious agents in the development of autoimmune diseases. Some of this interest is based on the concept of molecular mimicry as a causal mechanism. Molecular mimicry refers to the possible pathologic role of cross-reactive antibodies or T cells to a self-antigen that is structurally similar to, and thus shares epitopes with, a viral or other infectious agent. For most autoimmune diseases, however, evidence of molecular mimicry leading to disease is not conclusive.1819 Viruses and other infections also have a less-specific immune effect, stimulating toll-like receptors and proinflammatory cytokine secretion, which is another mechanism that has been postulated to influence autoimmune disease risk.20... 

Fig. 1. Transmission mechanisms. Strain barrier PrPc (circle) interacts with different strains of PrPSc (square or triangle). The replicated PrPSc is similar to the template. The 3F4 epitope is not recognized when it is in PrPSc, but is exposed after pardal denaturation by GdnHCI so that it is detected by the antibody. Antibody reactivity depends on the particular strain of PrP (Safar et aL, 1998). Species barrier when the template PrPSc contains unfavorable residues at the binding interface, the transformation of PrPc to Pr l>Sr does not occur. In vitro replication 35S label of PrPc is detected in PrPSc after replication in a medium containing GdnHCI (Kocisko et aL, 1994).

There is also considered to be a population of T suppressor cells which acts to down-regulate both T helper cells and B cells, whether through antigen-specific or idiotype-specific mechanisms. The epitopes on the lymphocyte receptor (id-iotype) recognized by the receptor on another lymphocyte (anti-idotype) can form a network of interactions through which suppression may be mediated. 

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