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Cell adhesion molecules (CAMs) are glycoproteins uniformly present on the cell surface. They are responsible for cell-to-cell and cell-to-extracellular environment interactions such as adhesion, growth, migration. They are expressed on the surface of the immune cells and take part in various inflammatory events. CAMs are divided into four groups: immunoglobulin superfamily, selectins, cadherins and integrins. They all share the same structure: CAMs are composed of three fragments – extracellular domain responsible for receiving signals from the extracellular space, transmembrane fragment and intracellular part which interacts with cytoskeleton. CAMs are present on cell-membrane in their native original cell-bound forms which may be released to body fluids as circulating or soluble forms. The soluble forms likely have the same potential of binding to their natural counterparts as the native forms. It is generally admitted that increased concentration of the soluble form reflects its overexpression on the cell surface. We hypothesized that the soluble forms could be a sort of truncated false saturators for their natural counterpart which finally reduce the triggered inflammatory cascade. They should be then considered a self-limiting negative feed-back mechanism of the CAM-activated inflammatory pathway. We present current data on the possible involvement of CAMS in various human pathologies with special emphasis on the diseases of the nervous system.

Cell adhesion molecules and their possible role in the pathology of the peripheral nerves – a review of the literature