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Stephan R. Targan

Researcher at Cedars-Sinai Medical Center

Publications -  577
Citations -  61849

Stephan R. Targan is an academic researcher from Cedars-Sinai Medical Center. The author has contributed to research in topics: Inflammatory bowel disease & Ulcerative colitis. The author has an hindex of 108, co-authored 545 publications receiving 58069 citations. Previous affiliations of Stephan R. Targan include University of Münster & Mount Sinai Hospital, Toronto.

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Defective generation of tetanus-specific antibody-producing B cells after in vivo immunization of Crohn's disease and ulcerative colitis patients.

TL;DR: There are in vivo humoral immune defects in inflammatory bowel disease, and antibody production by the B cells that spontaneously secrete tetanus-specific immunoglobulin G in vitro was highly variable and below normal in the majority of Crohn's disease and ulcerative colitis patients.
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Crohn's disease-associated genetic marker is seen in medically unresponsive ulcerative colitis patients and may be associated with pouch-specific complications.

TL;DR: The Crohn's disease-associated tumor necrosis factor microsatellite haplotype a2b1c2d4e1 may define a subgroup of medically unresponsive patients with ulcerative colitis who are predisposed to a higher incidence of pouch-specific complications after ileal pouch-anal anastomosis.
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HMPL-004 (Andrographis paniculata extract) prevents development of murine colitis by inhibiting T cell proliferation and TH1/TH17 responses

TL;DR: HMPL-004 inhibits the development of chronic colitis by affecting early T-cell proliferation, differentiation, and TH1/TH17 responses in a T- cell-driven model of colitis, presenting a unique mechanism of action.
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Expression and regulation of the chemokine receptor CXCR3 on lymphocytes from normal and inflammatory bowel disease mucosa.

TL;DR: Activation-dependent receptor regulation and alteration in receptor-bearing cells, primarily in MLN draining inflamed intestinal tissue, suggest an important role for this T-cell subset in the pathogenesis of human IBD.
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Anti-CD2O chimeric monoclonal antibody (rituximab) treatment of immune-mediated thrombocytopenia associated with Crohn's disease.

TL;DR: This is a report of successful and sustained response to anti-CD2O antibody treatment, rituximab, for IBD-associated thrombocytopenia, and suggests that therapies directed against B-lymphocytes may not be effective for the treatment of human IBD, they may possibly be detrimental.