scispace - formally typeset
K

Kenneth J. Gollob

Researcher at Santa Casa Hospital

Publications -  125
Citations -  5120

Kenneth J. Gollob is an academic researcher from Santa Casa Hospital. The author has contributed to research in topics: Immune system & Antigen. The author has an hindex of 37, co-authored 111 publications receiving 4638 citations. Previous affiliations of Kenneth J. Gollob include Centers for Disease Control and Prevention & Universidade Federal de Minas Gerais.

Papers
More filters
Journal ArticleDOI

Up-Regulation of Th1-Type Responses in Mucosal Leishmaniasis Patients

TL;DR: The data indicate that a poorly modulated T-cell response in mucosal leishmaniasis patients leads to production of high levels of proinflammatory cytokines, such as IFN-γ and TNF-α, as well as a decreased ability of IL-10 and TGF-β to modulate this response.
Journal ArticleDOI

Lack of interferon gamma receptor beta chain and the prevention of interferon gamma signaling in TH1 cells.

TL;DR: The ability of interferon gamma to inhibit the proliferation of type 2 T helper cells (TH2), but not that of type 1 (TH1) cells, suggests that helper cell subsets might differ in their activation of the IFN-gamma signaling pathway.
Journal ArticleDOI

An endogenous retrovirus mediating deletion of alpha beta T cells

TL;DR: A perfect genetic linkage is reported between Etc-1 and Mtv-9 and it is shown that EtC-1 is also involved in the I–E-dependent deletion of T cells bearing Vβ5.1 and Vβ11 domains.
Journal ArticleDOI

Current understanding of immunity to Trypanosoma cruzi infection and pathogenesis of Chagas disease.

TL;DR: It was demonstrated that a reduction in the anti-inflammatory cytokine IL-10 was associated with clinically significant chronic chagasic cardiomyopathy, and the components of the eicosanoid pathway such as thromboxane A2 and the lipoxins has been demonstrated to have profound effects as both pro- and anti- inflammatory factors.
Journal ArticleDOI

Decreased in situ expression of interleukin-10 receptor is correlated with the exacerbated inflammatory and cytotoxic responses observed in mucosal leishmaniasis.

TL;DR: The data identified distinct cytokine and cell population profiles for CL versus ML patients and provide a possible mechanism for the development of ML disease through the demonstration that low expression of IL-10 receptor is present in conjunction with a cytotoxic and inflammatory profile in ML.