EFFECTORS MECHANISMS OF INNATE CD8+ T CELLS (TIM CELLS)

VIANO, MARÍA ESTEFANÍA; STEMPI, CINTHIA CAROLINA; BAIGORRI RUTH; CERBÁN FABIO; RODRÍGUEZ-GALÁN, MA. CECILIA

Congreso; Reunión de Biociencias 2021; 2021

Innate CD8+ T cells (TIM cells) mature in the thymus as a differentlineage from conventional simple positive CD8+ thymocytes and areexported to SLO as a conventional T cell. TIM cells play a protectiverole during the early phase of infectious processes as reported forcertain bacteria, viral and parasite infections. We have previouslyreported that thymi from T. cruzi-infected mice are highly enrichedon TIM cells. Functionally, TIM cells act in a TCR-independent waybut can exert their cytotoxic capacity through the release of perforin/granzyme. It is also postulated that TIM cells can induce cell deaththrough the killing receptor NKG2D. NKG2D recognizes infectedcells expressing different families of ligands, especially RAE-1 receptors.However, this cytolytic mechanism is still poorly described.We evaluated the killing capacity of a bulk population of thymocytesobtained from T.cruzi-infected or control mice (efectors) whenco-cultured with peritoneal macrophages (PM) infected with T.cruzi(targets). As a read-out we evaluated 48h later, the number of parasiteeither inside macrophages (by IF) or in the culture supernatants72h later. In both cases, we observed a reduced number of parasitewhen macrophages were co-cultured with T.cruzi-infected thymocytes(<0,05).Interestingly, PM stimulation with different TLR agonists demonstrateup-regulation of RAE-1g only after PolyI:C but not after LPSor PGN stimulation (<0,05). Also, PM obtained from T.cruzi-infectedmice show significantly higher RAE-1g expression than PM fromcontrol mice (<0,05) becoming a possible target of NKG2D+ TIM cells.Our data intend to contribute in the understanding of the effectorsmechanisms of TIM cells.