J
Jesse M. Damsker
Researcher at National Institutes of Health
Publications - 41
Citations - 1719
Jesse M. Damsker is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Duchenne muscular dystrophy & Inflammation. The author has an hindex of 20, co-authored 39 publications receiving 1447 citations. Previous affiliations of Jesse M. Damsker include George Washington University & Washington University in St. Louis.
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Journal ArticleDOI
Th1 and Th17 cells
TL;DR: Recent studies report overlapping as well as differential roles of these cells in tissue inflammation, which suggests the existence of a more complex relationship between these two effector T‐cell subsets than has hitherto been suspected.
Journal ArticleDOI
VBP15, a novel anti-inflammatory and membrane-stabilizer, improves muscular dystrophy without side effects
Christopher R. Heier,Jesse M. Damsker,Qing Yu,Blythe C. Dillingham,Tony Huynh,Jack H. Van der Meulen,Arpana Sali,Brittany K. Miller,Aditi Phadke,Luana Scheffer,James L Quinn,Kathleen Tatem,Sarah Jordan,Sherry Dadgar,Olga Rodriguez,Chris Albanese,Michael E. Calhoun,Heather Gordish-Dressman,Jyoti K. Jaiswal,Edward M. Connor,John M. McCall,Eric P. Hoffman,Erica K.M. Reeves,Kanneboyina Nagaraju +23 more
TL;DR: Successful improvement of dystrophy independent of hormonal, growth, or immunosuppressive effects is demonstrated, indicating VBP15 merits clinical investigation for DMD and would benefit other chronic inflammatory diseases.
Journal ArticleDOI
Novel Approach to Inhibit Asthma-Mediated Lung Inflammation Using Anti-CD147 Intervention
William M. Gwinn,Jesse M. Damsker,Rustom Falahati,Ifeanyi Okwumabua,Ann E. Kelly-Welch,Achsah D. Keegan,Christophe Vanpouille,James J. Lee,Lindsay A. Dent,David Leitenberg,Michael Bukrinsky,Stephanie L. Constant +11 more
TL;DR: It is proposed that extracellular cyclophilins, via interaction with CD147, may contribute to the recruitment of leukocytes from the periphery into tissues during inflammatory responses, providing a novel mechanism whereby asthmatic lung inflammation may be reduced.
Journal ArticleDOI
Preferential chemotaxis of activated human CD4+ T cells by extracellular cyclophilin A.
TL;DR: It is shown that activatd human T lymphocytes express elevated levels of CD147, compared with resting T cells and that these activated T cells migrate more readily to CypA than resting cells, suggesting that cyclophilin‐CD147 interactions will be most potent when leukocytes are in an activated state, for example, during inflammatory responses.
Journal ArticleDOI
Targeting the chemotactic function of CD147 reduces collagen-induced arthritis.
Jesse M. Damsker,Ifeanyi Okwumabua,Tatiana Pushkarsky,Kamalpreet Arora,Michael Bukrinsky,Stephanie L. Constant +5 more
TL;DR: It is demonstrated that proinflammatory leucocytes, specifically neutrophils, monocytes and activated CD4+ T cells, lose their ability to migrate in response to cyclophilin A in vitro when treated with anti‐CD147 monoclonal antibody, suggesting that CD147–cyclophil in interactions might contribute to the pathogenesis of RA by promoting the recruitment of leucocyte into joint tissues.