Peripheral blood CD161⁺ T cells from asthmatic patients are activated during asthma attack and predominantly produce IFN-γ

In humans, T cells expressing the CD161 molecule NKR-P1A constitute around 20% of the circulating CD3⁺ cells and are potentially immunoregulatory in several diseases. Their role in asthma is not well known, but they could participate in asthma attacks. To determinate whether activation of CD161⁺ T cells and their cytokine production correlate with clinical status of asthma, we analysed blood samples from asthma attack patients (AAP) and stable asthma patients (SAP) in comparison with healthy non-atopic controls (HC). There was a significant higher baseline expression of CD69 on T cells from AAP and the difference was more notorious on CD161⁺ T cells; upregulation of CD69 was observed on both CD161^- and CD161⁺ T cells driven by Dermatophagoides pteronyssinus crude extract, whereas polyclonal stimulation with phorbol 12-myristate 13-acetate plus ionomycin predominantly induced IFN-γ but no IL-4, IL-5 and IL-13 by CD161⁺ T cells in all groups; upon polyclonal stimulation, there were more CD161⁺ T cells producing IFN-γ and less CD161^- T cells producing this cytokine, contrasting with the opposite results observed in SAP and HC groups. Our results indicate that, during asthma attack, CD161⁺ T cells are activated and are able to produce predominantly IFN-γ but no Th2 cytokines. We hypothesize that during an asthma attack, IFN-γ produced by CD161⁺ T cells could help to reestablish the Th1/Th2 equilibrium. These observations may contribute to the understanding of the immune mechanisms involved in asthma attacks.