Skip to main content
. 1998 Nov 10;95(23):13355–13357. doi: 10.1073/pnas.95.23.13355

Figure 1.

Figure 1

Model for the role of DSHP in the CTL response to EBV. (A) EBV-infected B cells secrete hIL-10 and vIL-10. These cytokines augment proliferation and survival of infected B cells, up-regulate the inhibitory receptor KIR on CTLs, and act on macrophages to inhibit T and NK cell function (not shown). During the CTL response to EBV in normal individuals, DSHP (green) attenuates inhibitory signals (red) from SHIP, CTLA-4, and/or KIR late in the immune response. This prolongs the response, allowing rapidly proliferating EBV-infected cells to be controlled. (B) In XLP patients, inhibitory signals (red) predominate in the absence of DSHP, and EBV-infected B cells escape immune surveillance.