Vasoactive Intestinal Peptide Inhibits Pathogenic Th17 Cells from Rheumatoid Arthritis Patients

Vasoactive Intestinal Peptide Inhibits Pathogenic Th17 Cells from Rheumatoid Arthritis Patients

A study published in the Journal of Leukocyte Biology indicates that in blood from rheumatoid arthritis (RA) patients, vasoactive intestinal peptide (VIP) shifts the activity of T cells towards a more T regulatory cell phenotype, and reduces the pathogenic profile of T helper (Th)17 cells.

The vasoactive intestinal peptide (VIP) is well-known for its immunoregulatory properties. This includes mostly anti-inflammatory actions, induction of Th2 cell polarization, and promotion of T regulatory functions (Ganea D, Gonzalez-Rey E & Delgado M, 2006).

Recent studies report that VIP reduces the development and severity of experimental arthritis and modulates Th17 cell activity (Delgado M et al., 2001; J Leceta et al., 2007).

Recent research points to a central role of Th17 cells in RA pathogenesis, and that these cells are key orchestrators of chronic inflammation in RA.

In the Journal of Leukocyte Biology study the authors studied CD4+CD45RO+ T cells from the blood of early RA patients under a Th-17 polarizing environment in the presence of VIP.

They demonstrated that 7 days of co-culture with VIP resulted in reduced levels of IL-22 production, and increased levels of IL-10 and IL-9 in the supernatants of Th cell cultures from early RA patients.

Of note, VIP also increased the levels of Foxp3 RNA expression and the Treg/Th17 ratio.

These results indicate that VIP may have promising effects in the early phase of RA targeting the inhibition of pathogenic Th17 cells,and favoring Treg cell differentiation.

Source: Journal of Leukocyte Biology, 2015. DOI: 10.1189/jlb.3A0714-327R

Read more: Journal of Leukocyte Biology

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