It has been well-established that T cells may be activated by a number of pathways in addition to the TcR-CD3 pathway. Studies of CD2 and sialophorin have established that both of these molecules may trigger T-cell proliferation and effector function. The studies described here have demonstrated that the interaction of CD2 with its naturally occurring ligand LFA-3 provides one signal for T-cell activation. They also have localized one region on the CD2 molecule necessary for LFA-3 binding. Furthermore, anti-sialophorin MAb has been shown to initiate both resting T-cell and thymocyte proliferation. The natural ligand for sialophorin, if one exists, remains to be identified. Both CD2 and sialophorin are expressed early in thymic ontogeny and may play a role in the regulation of thymic proliferation and differentiation. LFA-3 is expressed on thymic epithelial cells; anti-CD2 and anti-LFA-3 MAbs inhibit both thymocyte binding to thymic epithelial cells and thymocyte proliferation in response to LFA-3+ accessory cells and mitogen. Both the role of the sialophorin molecule and the mechanism by which the CD2/LFA-3 interaction regulates T-cell proliferation and T-cell repertoire development remain a current focus of active investigation.
|Number of pages||17|
|Journal||Immunology and Allergy Clinics of North America|
|State||Published - 1988|