Diminished IL-17A levels may protect filarial-infected individuals from development of rheumatoid arthritis and systemic lupus erythematosus.

Abstract

Nematode infections have been observed to inversely correlate with autoimmune disorders. Recently, we have shown the absence of filarial infection in patients with rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) who live in filarial-endemic areas. The mechanism(s) by which filarial-infected individuals are protected against the development of RA or SLE are unknown. In mice CIA, an experimental model for RA, ES-62, an execratory product of rodent filarial nematode , has been shown to improve arthritis through suppression of the IL-17 pathway. A total of 160 individuals, 40 each of endemic normal, filarial-infected cases, SLE and RA patients, from filarial-endemic areas, were enrolled in the study. Plasma levels of IL17-A, IFN-α and TNF-α were quantified by enzyme-linked immunosorbent assay (ELISA). RA and SLE patients displayed significantly higher plasma IL-17A, IFN-α and TNF-α levels compared to endemic normal and infected individuals. Furthermore, IL-17A levels were significantly low in participants with filarial infection compared to endemic controls ( p < 0.05). Interestingly, plasma IL-17A levels correlated inversely with circulating filarial antigen (CFA) ( p = 0.004, Spearman r = -0.51). Filarial infection was associated with low plasma IL-17A levels, a mechanism by which it possibly protects individuals in filarial-endemic areas from the development of autoimmune disorders like RA and SLE.