Fig. 1.

A model that correlates changes in the plasma membrane with TCR stimulation. In non-stimulated T-cells, the TCR is in monomeric form and its interaction with lipid rafts is transitory and unable to initiate signalling. Upon antigenic challenge, the reorganization of actin cytoskeleton results in formation of TCR microclusters and reduces the mobility of lipid rafts thus creating an environment conducive to long-lasting interactions. Concomitantly, the activity of Lck in lipid rafts increases owing to the action of a pool of CD45 molecules that moves to close proximity. These changes favour phosphorylation of ITAMs and initiation of signalling.