Death recep­tors were initi­ally cha­rac­te­ri­zed to induce apo­pto­sis after liga­tion with their cognate death ligand. Nowa­days, howe­ver, it is clear that death recep­tors have addi­tio­nal func­tions. We have recently inves­ti­ga­ted the influ­ence of death recep­tor CD95 and TRAIL on T cell acti­va­tion and define for the first time, that CD95 and TRAIL-​receptors sup­press T cell acti­va­tion when sti­mu­la­ted by death ligands during T cell pri­ming. This mecha­nism might con­tri­bute to immune eva­sion of viruses or other patho­gens, which induce death ligand expres­sion in tar­get cells after infec­tion.

GVHD is cha­rac­te­ri­zed by reci­pi­ent organ destruc­tion indu­ced by acti­va­ted T cells. Since acti­va­ted T cells stron­gly up-​regulate death ligands we are explo­ring whe­ther blo­cking of death ligand func­tions might serve as a pos­si­ble treat­ment option in GVHD pre­ven­tion. Destruc­tive func­tions of acti­va­ted T cells, howe­ver, can also be abro­ga­ted by sup­pres­sor cells. Myeloid-​derived sup­pres­sor cells (MDSCs) are an imma­ture popu­la­tion of mye­loid cells inhi­bi­ting T cell acti­va­tion, pro­li­fe­ra­tion and func­tion and are the­re­fore under inves­ti­ga­tion for GVHD-​prophylaxis. T cells do not repre­sent a uni­form popu­la­tion of cells but are sub­di­vi­ded in dif­fe­rent sub­po­pu­la­ti­ons due to their phe­no­type and func­tion. The impact of dif­fe­rent T cell sub­po­pu­la­ti­ons espe­cially Th9 cells on GVHD deve­lo­p­ment is stu­died.

The immune response after trau­ma­tic inju­ries is pre­do­mi­na­ted in the begin­ning by on over­whel­ming pro-​inflammatory response of the innate immune sys­tem, fol­lo­wed by a sup­pres­sion of the adap­tive immu­nity lea­ding to immu­no­sup­pres­sion and an enhan­ced risk for all types of infec­tions. At pre­sent, the impact of MDSCs on the course of disease and the immune response after trauma is not well defi­ned. Using murine trauma models we deter­mine the influ­ence of trauma on the induc­tion of MDSCs, define their poten­tial to modu­late T cell-​mediated immune respon­ses in order to cla­rify whe­ther inter­fe­rence with MDSC deve­lo­p­ment might be a the­ra­peu­tic option after trauma.