TAILIEUCHUNG - báo cáo hóa học:" Alpha-1 antitrypsin protein and gene therapies decrease autoimmunity and delay arthritis development in mouse model"

Tuyển tập các báo cáo nghiên cứu về hóa học được đăng trên tạp chí sinh học đề tài : Alpha-1 antitrypsin protein and gene therapies decrease autoimmunity and delay arthritis development in mouse model | Grimstein et al. Journal of Translational Medicine 2011 9 21 http content 9 1 21 TRANSLATIONAL MEDICINE RESEARCH Open Access Alpha-1 antitrypsin protein and gene therapies decrease autoimmunity and delay arthritis development in mouse model 11 11 2 23 2 3 Christian Grimstein Young-Kook Choi Clive H Wasserfall Minoru Satoh Mark A Atkinson Mark L Brantly Martha Campbell-Thompson2 Sihong Song1 Abstract Background Alpha-1 antitrypsin AAT is a multi-functional protein that has anti-inflammatory and tissue protective properties. We previously reported that human AAT hAAT gene therapy prevented autoimmune diabetes in non-obese diabetic NOD mice and suppressed arthritis development in combination with doxycycline in mice. In the present study we investigated the feasibility of hAAT monotherapy for the treatment of chronic arthritis in collagen-induced arthritis CIA a mouse model of rheumatoid arthritis RA . Methods DBA 1 mice were immunized with bovine type II collagen bCII to induce arthritis. These mice were pretreated either with hAAT protein or with recombinant adeno-associated virus vector expressing hAAT rAAV-hAAT . Control groups received saline injections. Arthritis development was evaluated by prevalence of arthritis and arthritic index. Serum levels of B-cell activating factor of the TNF-a family BAFF antibodies against both bovine bCII and mouse collagen II mCII were tested by ELISA. Results Human AAT protein therapy as well as recombinant adeno-associated virus rAAV8 -mediated hAAT gene therapy significantly delayed onset and ameliorated disease development of arthritis in CIA mouse model. Importantly hAAT therapies significantly reduced serum levels of BAFF and autoantibodies against bCII and mCII suggesting that the effects are mediated via B-cells at least partially. Conclusion These results present a new drug for arthritis therapy. Human AAT protein and gene therapies are able to ameliorate and delay arthritis development and

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