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[M. Immunology-31]



                Bee Venom Phospholipase A2 alleviates collagen-induced


                polyarthritis by inducing Foxp3+ Treg cell polarization in


                                                        mice



                          Gwang Muk Choi¹, Riwon Hong¹˙², Hyunsu Bae¹˙², Dae Hyun Hahm¹˙³


           ¹Department of Biomedical Sciences, Graduate School, Kyung Hee University, Seoul 02447, Republic of Korea,

          ²Department of Science in Korean Medicine, Graduate School, Kyung Hee University, Seoul 02447, Republic of
          Korea, ³Department of Physiology, College of Medicine, Kyung Hee University, Seoul 02447, Republic of Korea




        In the present study, bee venom phospholipase A2 (bvPLA2), a BV enzyme catalyzing the release of membrane

        arachidonic acid, is suggested to be a novel anti-inflammatory BV mediator stimulating the CD25+ Foxp3+ Treg
        cell  polarization.  To  verify  this  hypothesis,  anti-arthritic  effect of  bvPLA2  was evaluated in  a  mouse  model  of

        rheumatoid arthritis (CIA). An experimental arthritis was induced by 2-week-interval double injections of type II
        collagen emulsified in complete (1st) and incomplete Freund’s adjuvant (2nd injection) to the base of the tail. After

        2nd injection, bvPLA2 (0.1, 0.5, 1.0 mg/kg) was i.p. injected every two days for 5 weeks. Arthritic behaviors were
        significantly alleviated, and histological and micro-CT images of arthritic joints were highly coincident with their

        behaviors. Anti-arthritic effects of bvPLA2 became extinct by 0.25 mg/kg anti-CD25 IgG and 10 μg/kg P60, a peptide
        inhibitor of Treg, as regards arthritic behaviors. Interestingly, it was observed in flow cytometric analysis of major T

        cell  subsets from  spleen that  Tregs were  completely  depleted by the anti-CD25 IgG treatment, not  by P60.  In
        summary, bvPLA2 have a significant anti-inflammatory and anti-arthritic activity in the CIA mouse model through

        the modulation of development and function of Treg.
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