The contribution of the CTLA-4/CD28/B7-2 pathways to the pathogenesis of systemic inflammatory response in patients with pneumonia associated with A/H1N1 influenza

Abstract

Aims. To evaluate the contribution of the CTLA-4/CD28/B7-2 signaling pathways to the development of systemic inflammatory response in patients with pneumonia associated with influenza A/H1N1.

Materials and methods. 100 patients with pneumonia associated with A/H1N1 influenza were evaluated. 30 of these patients had severe pneumonia and 70 had non-severe pneumonia. The diagnosis of influenza A/H1N1 was confirmed by a positive result of PCR test. For diagnosis and assessment of pneumonia severity, the CURB/CRB-65 scales, SMART-COP, 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 regarded as "severe") were used. The plasma concentration of the B7-2 molecule was measured by cytometry on a Beckman Coulter analyzer using LEGENDplex™ HU Immune Checkpoint Panel 1 multiplex assay kits.

Results. In patients with severe pneumonia associated with A/H1N1 influenza, the concentration of B7-2 was increased 3.4 times and in patients with non-severe pneumonia, 2.8 times compared to the control group. At the same time, there were no differences in the concentration of B7-2 between subgroups of patients with severe pneumonia associated with A/H1N1 influenza with different outcomes of the disease, recovery or a fatal outcome.

Conclusion. A statistically significant increase in the concentration of B7-2 in pneumonia patients with A/H1N1 influenza may likely contribute to the involvement of the CTLA-4 and CD28 signaling pathways in the adaptive immune cascade, which forms a pro-inflammatory background for the development of a critical condition with simultaneous activation of the inhibitory component of T-cell response regulation.