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Complement‐activated human endothelial cells stimulate increased polyfunctionality in alloreactive T cells

Antibody‐mediated deposition of complement membrane attack complexes (MACs) on IFN‐γ‐primed human endothelial cells (ECs) triggers autocrine/paracrine IL‐1β‐mediated EC activation and IL‐15 transpresentation to alloreactive effector memory T cells (TEM), changes that enable ECs to increase T cell proliferation and cytokine release. Here, we report the use of single‐cell microchip 32‐plex proteomics to more deeply assess the functionality of the activated T cells and dependence upon EC‐derived signals. Compared to control ECs, MAC‐activated human ECs increase both the frequency and degree of polyfunctionality among both CD4+ and CD8+‐proliferated TEM, assessed as secreted proteins. IFN‐γ and TNF‐α remain the predominant cytokines made by alloreactive TEM, but a few CD4+ TEM also made IL‐4 while more CD8+ TEM made perforin and granzyme B. Increased polyfunctionality was attenuated by treatment of the MAC‐activated ECs with anti‐IL‐15 blocking antibody more effectively than IL‐1 receptor blockade. The increased polyfunctionality of T cells resulting from interactions with MAC‐activated ECs may further link binding of donor‐specific antibody to T cell–mediated allograft pathologies.