Changes are also seen in the cell-adhesion molecules and receptors expressed by effector T cells. They lose cell-surface L-selectin and therefore cease to recirculate through lymph nodes. Instead, they express glycans that serve as ligands for Pand E-selectins (for example, P-selectin glycoprotein-1, or PSGL-1), which are upregulated on inflamed vascular endothelial cells and
Fig. 9.26 Effector T cells can respond to their target cells effector cell status (central panel). once the cells have differentiated without co-stimulation. a naive T cell that recognizes antigen on into effector T cells, any encounter with specific antigen triggers the surface of an antigen-presenting cell and receives the required their effector actions without the need for co-stimulation. Thus, as two signals (arrows 1 and 2, left panel) becomes activated, and it illustrated here, a cytotoxic T cell can kill any virus-infected target both secretes and responds to IL-2. IL-2 signaling enhances clonal cells, including those that do not express co-stimulatory molecules. expansion and contributes to the differentiation of the T cells to allow effector T cells to roll on the blood vessels at sites of inflammation. They also express higher levels of LFA-1 and CD2 than do naive T cells, as well as the integrin VLA-4, which allows them to bind to vascular endothelium bearing the adhesion molecule VCAM-1, which is also expressed on the inflamed endothelium. This allows effector T cells to exit the bloodstream and enter sites of infection, where they orchestrate the local immune response. These changes in the T-cell surface are summarized in Fig. 9.27, and will be discussed further in Chapter 11.
Fig. 9.27 Activation of T cells changes the expression of several cell-surface molecules. The example here is a Cd4 T cell. resting naive T cells express L-selectin, through which they home to lymph nodes, but express relatively low levels of other adhesion molecules such as Cd2 and LFa-1. upon activation, expression of L-selectin ceases and, instead, expression of ligands for pand e-selectins are induced (e.g., psGL-1), which allow the activated T cells to roll on pand e-selectins expressed on endothelium at sites of inflammation. Increased amounts of the integrin LFa-1 are also produced, which is activated to bind its ligands, ICaM-1 and ICaM-2. a newly expressed integrin called vLa-4, which allows T cells to arrest on inflamed vascular endothelium, ensures that activated T cells enter peripheral tissues at sites where they are likely to encounter infection. activated T cells also have on their surface a higher density of the adhesion molecule Cd2, increasing the avidity of their interaction with potential target cells, as well as a higher density of the adhesion molecule Cd44. By alternative splicing of the rna transcript of the Cd45 gene, a change occurs in the isoform of Cd45 that is expressed, with activated T cells expressing the Cd45ro isoform, which associates with the T-cell receptor and Cd4. This change makes the T cell more sensitive to stimulation by low concentrations of peptide:MhC complexes. Finally, the sphingosine 1-phosphate receptor 1(s1pr1) is expressed by resting naive T cells, allowing the egress from lymphoid tissues of cells that do not become activated (see Fig. 9.11). downregulation of s1pr1 for several days after activation prevents T-cell egress during the period of proliferation and differentiation. after several days, it is expressed again, allowing effector cells to exit from the lymphoid tissues.
9-19 CD8 T cells can be activated in different ways to become cytotoxic effector cells.