He 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 (rAAVhAAT). 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, 4-((2-Hydroxyethyl)(methyl)amino)benzaldehyde 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 reduce autoimmunity, indicating promising potential of these PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/8086425 therapies 3-Amino-1H-indazole-4-carbonitrile as a new treatment strategy for RA.Background Rheumatoid arthritis (RA) is a systemic autoimmune disease, characterized by chronic joint inflammation and synovial hyperplasia leading to bone and joint destruction. The life expectancy is lowered and quality of life is decreased in RA patients. So far little is known about the actual disease PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/13485127 initiating stimulus; however, extensive research over the last decades have shown that multiple genetic as well as environmental factors interact and trigger the onset of RA [1,2]. The autoimmune inflammation of RA is maintained by inappropriate action of* Correspondence: shsong@ufl.edu Contributed equally 1 Department of Pharmaceutics, University of Florida, Gainesville, FL 32610, USA Full list of author information is available at the end of the articlemacrophages, B-cells, T-cells, and other types of cells leading to dysregulated cytokine/chemokine production. The synovial inflammation is caused by infiltration and proliferation of activated immune cells including neutrophils, macrophages, fibroblasts, mast cells, NK cells, NKT cells, T-cells as well as plasma cells [3]. Progressive joint and bone destruction is mediated through the activities of osteoclasts, chondrocytes, synovial fibroblasts and cytokine induction of destructive enzymes, chiefly matrix metalloproteinases (MMP) [4]. Current therapy mainly aims to inhibit the biological function of tumor necrosis factor-alpha (TNF-a) and lymphocyte proliferation. Due to ineffectiveness of anti-TNF-a therapy in certain patients and various side effects of methotrexate which inhibits lymphocytes proliferation, there is?2011 Grimstein et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.Grimstein et al. Journal of Translational Medicine 2011, 9:21 http://www.translational-medicine.com/content/9/1/Page 2 ofstill the need to identify new target molecules/pathways and to develop new treatment [5].