Rheumatoid arthritis (RA) is a chronic autoimmune condition characterized, among others, by tissue damage and activation/differentiation of proinflammatory lymphocytes. Accordingly, several studies have concluded that type 17 T helper (Th17) cells seem to have an important role in the pathogenesis of this condition. However, the strategy for the identification and analysis of proinflammatory Th17 cells in those studies has not been consistent and has usually been different from what was originally described. Therefore, we decided to evaluate the levels of Th17 cells in patients with RA employing an extended immune phenotype by using an eight-color multiparametric flow cytometry analysis. For this purpose, blood samples were obtained from 30 patients with RA and 16 healthy subjects, and the levels of Th17 and type 22 helper (Th22) lymphocytes were analyzed as well as the in vitro differentiation of peripheral blood mononuclear cells into Th17 lymphocytes induced by interleukin-23 (IL-23) and IL-1β. We found significant enhanced levels of total Th17 lymphocytes (defined as CD4⁺IL-17⁺) as well as enhanced numbers of their pathogenic (defined as CD4⁺CXCR3⁺IL-17⁺IL-22⁺CD243⁺CD161⁺IFN-γ⁺IL-10^-) and nonpathogenic (CD4⁺CXCR3⁺IL-17⁺IL-22^-CD243^-CD161^-IFN-γ^-IL-10⁺) cell subsets in patients with RA. Likewise, the number of Th22 (CD4⁺CXCR3^+/-IL-17^-IL-22⁺) was also increased in these patients compared to healthy controls. However, the in vitro induction/differentiation of pathogenic Th17 cells showed similar results in controls and patients with RA. Likewise, no significant associations were detected in patients with RA between the levels of Th17 or Th22 cells and clinical or laboratory parameters. Our data indicate that patients with RA show enhanced blood levels of the different subsets of Th17 cells and Th22 lymphocytes tested in this study and suggest that these levels are not apparently associated with clinical or laboratory parameters.

We sought to evaluate the effect of endodontic-causative microorganisms of primary infections on mononuclear cells such as CD14⁺, CD4⁺, CD8⁺, CD19⁺ and Tregs Foxp3⁺. Facultative anaerobic microorganisms were isolated from radicular conducts and peripheral blood samples, which were taken from patients with primary infections. Cellular cultures were performed with peripheral blood mononuclear cells (PBMC) with and without Actinomyces spp. and Streptococcus spp. during 48, 72, and 96 h of contact in culture (concentration 5 × 10⁵ cells/well) in a round plate bound with 48 wells. Later, PBMC was collected for analysis by flow cytometry, with the monoclonal antibodies αCD14, αCD4, αCD8, αCD19 and αFoxp3, and acquired using an FACSCanto II cytometer. The supernatant of cellular cultures was analyzed for the quantification of inflammatory cytokines. Data analysis was performed in FlowJo v10.8.2 and FCAPArray software, and statistical analysis was performed using GraphPad v5.0. software. We observed an increase in the percentage of CD14⁺ cells in patients at different hours of cellular culture in the presence of both Actinomyces spp. and Streptococcus spp. microorganisms, compared to healthy controls. This study demonstrates the role played by the innate immune system in the pathogeny of endodontic primary infections, explaining the effects that generate the more common microorganisms in this oral pathology.

The function of NK cells in cancer and viral infections is well documented and understood. NK cell activity, including cytokine secretion, cytotoxic activity, and the coordination of inhibitory and activating receptors, linking innate and adaptive immunity, among others, has been examined for numerous pathogens, including parasites, bacteria, and viruses. The emergence of the SARS-CoV-2 health crisis has exposed a deficiency in understanding the previously elucidated mechanisms; the rationale for the reported variability in symptomatology among COVID-19 patients is extensive and intricate. It is evident that NK cells exert a significant influence on symptom severity, and their absence, with the presence or absence of their surface receptors, elicits a tailored response to the virus. This overview examines the impact of NK cells on the progression of several viral diseases, emphasizing their involvement in the pathogenesis of SARS-CoV-2 via the activation of surface receptors.