Results 41 to 50 of about 17,630,315 (317)

Tim-3, Lag-3, and TIGIT [PDF]

open access: yes, 2017
Co-inhibitory receptors play a key role in regulating T cell responses and maintaining immune homeostasis. Their inhibitory function prevents autoimmune responses but also restricts the ability of T cells to mount effective immune responses against tumors or persistent pathogens.
Joller, Nicole, Kuchroo, Vijay K.
openaire   +3 more sources

Targeting Tim-3 and PD-1 pathways to reverse T cell exhaustion and restore anti-tumor immunity

open access: yesJournal of Experimental Medicine, 2010
The immune response plays an important role in staving off cancer; however, mechanisms of immunosuppression hinder productive anti-tumor immunity. T cell dysfunction or exhaustion in tumor-bearing hosts is one such mechanism.
K. Sakuishi   +5 more
semanticscholar   +1 more source

STIMULUS-MDS2 design and rationale: a phase III trial with the anti-TIM-3 sabatolimab (MBG453) + azacitidine in higher risk MDS and CMML-2.

open access: yesFuture Oncology, 2023
Patients with higher-risk myelodysplastic syndromes (MDS) and chronic myelomonocytic leukemia (CMML) unfit for hematopoietic stem cell transplantation have poor outcomes.
A. Zeidan   +8 more
semanticscholar   +1 more source

Increased frequency of Tim-3 expressing T cells is associated with symptomatic West Nile virus infection [PDF]

open access: yes, 2014
More than a decade after West Nile virus (WNV) entered North America, and despite a significant increase in reported cases during the 2012 and 2013 seasons, no treatment or vaccine for humans is available.
Busch, Michael P   +9 more
core   +3 more sources

Dok-3 deficient mice display different immune clustering and Tim-3 expression

open access: yesEuropean Journal of Medical Research, 2019
Background Dok-3 has been shown to play an important role in immune system. Tim-3 also has been recognized as an important immune regulator which involves in many diseases. The relationship of them is still unclear.
Wenjiang Yan   +7 more
doaj   +1 more source

TIM-3 does not act as a receptor for galectin-9. [PDF]

open access: yesPLoS Pathogens, 2013
T cell immunoglobulin and mucin protein 3 (TIM-3) is a type I cell surface protein that was originally identified as a marker for murine T helper type 1 cells. TIM-3 was found to negatively regulate murine T cell responses and galectin-9 was described as
Judith Leitner   +5 more
doaj   +1 more source

Phase I/Ib Clinical Trial of Sabatolimab, an Anti–TIM-3 Antibody, Alone and in Combination with Spartalizumab, an Anti–PD-1 Antibody, in Advanced Solid Tumors

open access: yesClinical Cancer Research, 2021
Purpose: Sabatolimab (MBG453) and spartalizumab are mAbs that bind T-cell immunoglobulin domain and mucin domain-3 (TIM-3) and programmed death-1 (PD-1), respectively.
G. Curigliano   +18 more
semanticscholar   +1 more source

Interrogating glioma-M2 macrophage interactions identifies Gal-9/Tim-3 as a viable target against PTEN-null glioblastoma

open access: yesScience Advances, 2022
Genomic alteration can reshape tumor microenvironment to drive tumor malignancy. However, how PTEN deficiency influences microenvironment-mediated cell-cell interactions in glioblastoma (GBM) remains unclear.
X. Ni   +13 more
semanticscholar   +1 more source

Human Galectin-9 Is a Potent Mediator of HIV Transcription and Reactivation. [PDF]

open access: yes, 2016
Identifying host immune determinants governing HIV transcription, latency and infectivity in vivo is critical to developing an HIV cure. Based on our recent finding that the host factor p21 regulates HIV transcription during antiretroviral therapy (ART),
Abdel-Mohsen, Mohamed   +17 more
core   +8 more sources

Tim-3 expression in cervical cancer promotes tumor metastasis.

open access: yesPLoS ONE, 2013
BackgroundT cell immunoglobulin mucin-3 (Tim-3) has been identified as a negative regulator of anti-tumor immunity. Recent studies highlight the important role of Tim-3 in the CD8(+) T cell exhaustion that takes place in both human and animal cancer ...
Yang Cao   +7 more
doaj   +1 more source

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