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Sohail Saleem

Researcher at Emory University

Publications -  9
Citations -  730

Sohail Saleem is an academic researcher from Emory University. The author has contributed to research in topics: CD28 & Glomerulonephritis. The author has an hindex of 8, co-authored 8 publications receiving 723 citations. Previous affiliations of Sohail Saleem include Veterans Health Administration.

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Journal Article

IFN-gamma is critical for long-term allograft survival induced by blocking the CD28 and CD40 ligand T cell costimulation pathways.

TL;DR: It is found that perioperative blockade of the CD28 and/or CD40 ligand T cell costimulation pathways induces long-term skin and heart allograft survival in IFn-gamma+/+ recipients but fails to do so in IFN-Gamma-/- mice or in wild-type mice treated with IFN -gamma-neutralizing Ab at the time of transplantation.
Journal Article

Blocking the CD28-B7 T cell costimulation pathway induces long term cardiac allograft acceptance in the absence of IL-4.

TL;DR: It is reported in this study that long term survival (>100 days) of fully allogeneic grafts can be induced readily in IL-4 -/- recipients treated with a short course of CTLA4Ig, and it is demonstrated that IL- 4 -/- mice are deficient in Th2-type cytokine expression following in vitro or in vivo allostimulation.
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Acute rejection of vascularized heart allografts in the absence of IFNgamma.

TL;DR: It is demonstrated that IFNgamma is not required for acute cellular rejection of fully allogeneic murine hearts and proposed that non-DTH mechanisms of allograft destruction could be enhanced in the absence of IFNGamma and thus lead to robust acute rejection.
Journal ArticleDOI

Interferon-gamma is necessary for initiating the acute rejection of major histocompatibility complex class II-disparate skin allografts.

TL;DR: The data demonstrate that IFNgamma is not necessary for generating effector mechanisms associated with acute transplant rejection but that it is required for initiating alloimmune responses to MHC class II-disparate skin grafts.
Journal Article

Increased susceptibility to immunologically mediated glomerulonephritis in IFN-gamma-deficient mice.

TL;DR: Evidence is provided that endogenous IFN-gamma has a protective role in immunologically mediated glomerulonephritis initiated by foreign Ags and mount a stronger cellular immune response (cutaneous delayed-type hypersensitivity reaction) to sheep IgG than IFN -gamma+/+ mice.