Abstract
The process of adhesion has been described in the medical literature for more than 100 years as a characteristic component of all forms of inflammation. Over the past few decades, multiple investigators have defined series of families of adhesion molecules that provide for intimate cell-cell contact and facilitate interactions among another series of activation molecules. To this end, the process of adhesion is intimately associated with activation and there has been some debate as to whether certain molecules provide for selective adhesion or for selective activation [1–7]. For instance, the adhesive interactions between MHC molecules and the T cell receptor, discussed in detail in Chapter X are critical for the activation of lymphocytes. But these interactions are of very low affinity and thus require the function of families of high affinity adhesion molecules to enable close approximation of these molecules and activation events. Furthermore, biological processes have evolved to facilitate these processes in as much as the interaction between cognate antigen and the T cell receptor is a process that facilitates the expression of high affinity adhesion molecules; and disruption of adhesion (such as ICAM-1-mediated adhesion, discussed below) may dysregulate activation. To this end it must be emphasized that adhesion events interrelate with activation responses and it is important to consider the entire adhesion process as fundamental to any bidirectional cell-cell activation response.
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Frank, M.H., Briscoe, D.M. (2001). Monoclonal Antibody Targeting of Adhesion Molecules. In: Sayegh, M.H., Remuzzi, G. (eds) Current and Future Immunosuppressive Therapies Following Transplantation. Springer, Dordrecht. https://doi.org/10.1007/978-94-010-1005-4_14
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DOI: https://doi.org/10.1007/978-94-010-1005-4_14
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