Activity of the inhibitory signaling pathway of T-cell immunoglobulin and mucin-domain-3 (Tim-3) in patients with pneumonia associated with influenza A/H1N1
Abstract
Background. One of the pathophysiological components of critical conditions is systemic inflammation. The innate and adaptive immune response cascade underlies the systemic inflammatory response and proceeds in two stages, from a hyperinflammatory systemic response to an anti-inflammatory compensatory phase and immunosuppression. The search for markers predicting the severity of critical conditions and possible ways of their correction remains an important scientific direction.
Aim. To evaluate the activity of the Tim-3 inhibitory signaling pathway in patients with pneumonia associated with influenza A/H1N1.
Materials and methods. 85 pneumonia patients with influenza A/H1N1 were evaluated. Of these patients, 30 patients had severe pneumonia and 55 had non-severe pneumonia. The diagnosis of influenza A/H1N1 was confirmed by a positive PCR test. The CURB/CRB-65 scales were used to diagnose and assess the severity of pneumonia; SMART-COP, as well as the Federal clinical guidelines of the Ministry of Health of the Russian Federation "Community-acquired pneumonia in adults", 2019 and the IDSA/ATS criteria. In the presence of one "major" or three "minor" criteria, pneumonia was considered "severe". The plasma concentration of the Tim-3 molecule was determined by flow cytometry with a Beckman Coulter (USA) analyzer using LEGENDplex™ HU Immune Checkpoint Panel Beckman Coulter (USA) multiplex analysis kits.
Results. It was found that in patients with severe pneumonia and influenza A/H1N1, the Tim-3 concentration was increased twofold compared to the control, while in the group of patients with severe pneumonia and influenza A/H1N1 who had a fatal outcome, the Tim-3 concentration was increased even more, by 2.3 times.
Conclusion. A statistically significant increase in the Tim-3 concentration in patients with severe pneumonia associated with A/H1N1 influenza indicates the involvement of the Tim-3 signaling pathway in the immunological cascade that inhibits the T-cell response and is associated with the severity of the condition and mortality.