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Retroviral Glycoprotein-Mediated Immune Suppression via the potassium Channel KCa3.1- A new strategy for treatment of Inflammatory Bowel Diseases.

Background and Purpose: Peptides derived from retroviral envelope
proteins have been shown to possess a wide range of immunosuppressive
and anti-inflammatory activities. We have previously reported
identification of such a peptide derived from the envelope protein coded
by a human endogenous retrovirus (HERV). In this study we assessed
effects of this peptide treatment on inhibition of immune response in
the DSS-induced mice model of colitis. Furthermore, we identified that
in vitro the peptide inhibits the KCa3.1 potassium channel, a
potential target for therapy of immune diseases. Experimental Approach:
We characterized an immunosuppressive peptide ENV59, from a specific
HERV envelope protein, in vivo effects on inflammation control in
acute colitis mice model and in vitro on the production of
pro-inflammatory cytokines. Furthermore, we described in vitro
ENV59-GP3 effects with respect to potency of inhibition on KCa3.1
channels and calcium influx. Key Results: ENV59-GP3 peptide treatment
showed reduction of the disease score in the DSS-induced acute colitis
mice model, which was comparable to effects of the KCa3.1 channel
blocker NS6180. Analysis of cytokine production from DSS-mice model
treated animals revealed equipotent inhibitory effects of the ENV59-GP3
and NS6180 compounds on the production of IL-6, TNF-α, IL-1β. Patch
clamp studies show that the peptide ENV59-GP3 is a blocker of the
potassium channel KCa3.1. Conclusion and Implications: Env59-GP3
represents KCa3.1 channel inhibitor underlining the implications of
using virus derived channel blockers for treatment of autoimmune
diseases. There are no drugs with a similar mechanism of action
currently on the market.