scispace - formally typeset
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.

Papers
More filters
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

Novel Approach to Inhibit Asthma-Mediated Lung Inflammation Using Anti-CD147 Intervention

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.

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.