{Reference Type}: Journal Article
{Title}: A Snapshot of T Cell Subset Cytokines in Pemphigus Vulgaris: A Cross-Sectional Study.
{Author}: Singh PK;Das S;Rai G;Ansari MA;Dar SA;Singh T;Pandhi D;
{Journal}: Cureus
{Volume}: 14
{Issue}: 10
{Year}: Oct 2022
暂无{DOI}: 10.7759/cureus.29890
{Abstract}: OBJECTIVE: The purpose of this study was to assess the serum levels of cytokines produced by the Th1 (IFN-γ, IL-12), Th2 (IL-4), Th17 (IL-6, IL-17A, IL-23), and Treg (IL-10 and TGF-β) pathways in individuals with active pemphigus vulgaris (PV) and to determine whether these levels were correlated with the severity of the disease condition.
METHODS: This study was conducted with 90 individuals, of which 50 were PV patients and 40 healthy individuals (age and gender-matched) as controls. Serum samples were collected and tested for cytokine levels by ELISA (enzyme-linked immunosorbent assay). The cytokine levels in the serum of PV patients and healthy controls were compared statistically using the Mann-Whitney test for nonparametric samples. The strength of the association between the variables was evaluated using the Spearman correlation test.
RESULTS: The mean serum levels of IFN- γ (p < 0.001), IL-6 (p < 0.001), IL-10 (p < 0.001), IL-12 (p < 0.05), and IL-17 (p < 0.001) were significantly higher and TGF-β were significantly low in the PV patients than those observed in the control group. The mean concentration of serum IL-4 in patients with PV did not differ from those in the control group.
CONCLUSIONS: In active PV, the Th1 and Th17 pathways are involved in the development and progression of the disease, whereas the Th2 pathway is blocked. Both of these pathways play a significant role in the disease. It is possible that the Treg pathway acts as an antagonist to the Th1 and Th17 pathways, which would cause the disease to become more localised. This study lays the foundation for a better understanding of the aetiology of PV and implies that cytokines could be used as potential therapeutic targets and disease activity biomarkers.