Answers are grounded in this paper and cite their sources.
The function of purified ICAM-1 in costimulating CD4+ and CD8+ T cell responses has been directly compared to that of B7-1 in a model system that minimizes contributions of other receptor-ligand interactions. While B7-1 costimulates both subsets of T cells, ICAM-1 is much more effective in the costimulation of CD8+ cells. ICAM-1 also synergizes with B7-1 for the induction of IL-2 production in CD8+ but not CD4+ T cells. These differences are not explained by differences in LFA-1 receptor expression on the two subsets of T cells. The CD8+ T cell response to ICAM-1 costimulation is associated with increased proliferation and IL-2 production at levels similar to those seen with B7-1 costimulation, but clonal expansion in response to ICAM-1 is not as great due to decreased cell survival. ICAM-1-mediated costimulation is effective for both naive and memory CT8+ T cells, is independent of CD28 engagement, and does not appear to be due solely to effects on adhesion. These results suggest that ICAM-1-dependent, B7-independent costimulation may be important in initiating a CTL response to class I antigen presented by cells that are not professional APC.
No takes yet. Share an insight, caveat, or question.
Deeths et al. (1999) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: