Neutrophils enhance gammadelta T cell activation triggered by anti-CD3 antobodies

TOWSTYKA, NADIA YASMÍN; BORGE, MERCEDES; SABBIONE, FLORENCIA; GIORDANO, MIRTA; GEFFNER, JORGE; TREVANI, ANALÍA; JANCIC, CAROLINA

Mar del Plata

Congreso; 62 Reuión Anual de la Sociedad Argentina de Inunología; 2014

Sociedad Argentina de Inmunología

gd T cells act as early sensors of cellular stress and infection; they use both, the TCR and additional activating receptors (i.e. NKG2D, TLRs), to respond to stress and/or infection-induced ligands. Furthermore, gd T cells play an important role in linking the innate and adaptive immunity. gd T lymphocytes modulate the function of neutrophils; and growing evidence supports a critical role of gd T cells in the recruitment and activation of neutrophils at the sites of infection. We previously reported that neutrophils suppress gd T cell activation induced by the specific agonist HMBPP, in a ROS-dependent manner. Now, we analyzed whether neutrophils were able to modulate the phenotype and function of human blood gd T cells activated by anti-CD3 antibodies. For this purpose, we analyzed the expression of T cell activation markers, CD25 and CD69 by flow cytometry and the production of IFN-g by ELISA. In this study, we found that the up-regulation of CD25 (p<0.05, n=6) and CD69 (p<0.05, n=6) expression, and the production of IFN-g (p<0.05, n=5) by activated gd T cells was increased in the presence of neutrophils. It was reported that IL-18 enhances the activation of stimulated gd T cells by different stimuli. Since neutrophils produce IL-18, we decided to evaluate the plausible role of this cytokine in the potentiation of gd T cell activation by neutrophils. Treatment of neutrophils with YVAD-CMK (a specific inhibitor of caspase-1) did not prevent the increase in gd T cell activation induced by neutrophils, showing that IL-18 was not involved. Our results indicate that neutrophils potentiate the activation of gd T cells stimulated through CD3/TCR pathway; contrasting with the inhibitory effect exerted by neutrophils when gd T cells are stimulated with HMBPP. The potentiation of gd T cell activation is not dependent on the presence of IL-18. We are currently investigating the mechanism/s involved in the enhancement of activated-gd T cell responses by neutrophils.