Results 31 to 40 of about 12,148,459 (347)

Mitochondrial Oxidative Phosphorylation Regulates the Fate Decision between Pathogenic Th17 and Regulatory T Cells

open access: yesCell Reports, 2020
Summary: Understanding metabolic pathways that regulate Th17 development is important to broaden therapeutic options for Th17-mediated autoimmunity.
Boyoung Shin   +6 more
doaj   +1 more source

TCR-independent functions of Th17 cells mediated by the synergistic actions of cytokines of the IL-12 and IL-1 families. [PDF]

open access: yesPLoS ONE, 2017
The development of Th17 cells is accompanied by the acquisition of responsiveness to both IL-12 and IL-23, cytokines with established roles in the development and/or function of Th1 and Th17 cells, respectively. IL-12 signaling promotes antigen-dependent
Yun Kyung Lee   +5 more
doaj   +1 more source

SKI Expression Suppresses Pathogenic Th17 Cell Response and Mitigates Experimental Autoimmune Encephalomyelitis

open access: yesFrontiers in Immunology, 2021
Pathogenic Th17 cells are critically involved in many autoimmune diseases, while non-pathogenic Th17 cells are more immune regulatory. Understanding the mechanisms of the induction and maintenance of pathogenic Th17 cells will benefit the development of ...
Ping Li   +6 more
doaj   +1 more source

Ovariectomy induces bone loss via microbial-dependent trafficking of intestinal TNF+ T cells and Th17 cells.

open access: yesJournal of Clinical Investigation, 2021
Estrogen deficiency causes a gut microbiome-dependent expansion of BM Th17 cells and TNF-α-producing T cells. The resulting increased BM levels of IL-17a (IL-17) and TNF stimulate RANKL expression and activity, causing bone loss.
Mingcan Yu   +8 more
semanticscholar   +1 more source

PKM2-dependent metabolic skewing of hepatic Th17 cells regulates pathogenesis of non-alcoholic fatty liver disease

open access: yesCell Metabolism, 2021
SUMMARY Emerging evidence suggests a key contribution to non-alcoholic fatty liver disease (NAFLD) pathogenesis by Th17 cells. The pathogenic characteristics and mechanisms of hepatic Th17 cells, however remain unknown.
Maria E. Moreno-Fernandez   +20 more
semanticscholar   +1 more source

Preferential recruitment of Th17 cells to cervical cancer via CCR6-CCL20 pathway. [PDF]

open access: yesPLoS ONE, 2015
Our previous studies suggest that Th17 cells accumulate within tumor tissues and correlate with recurrence of cervical cancer patients. However, the source of the increased tumor-infiltrating Th17 cells remains poorly understood.
Qing Yu, Xiang-ming Lou, Yan He
doaj   +1 more source

Th17 effector cells support B bell responses outside of germinal centres [PDF]

open access: yes, 2012
Th17 cells are pro-inflammatory CD4+T cells, which are important in immune responses against fungal pathogens and extracellular bacteria and have also been implicated in various autoimmune syndromes.
David R Withers   +39 more
core   +1 more source

Induction of intestinal Th17 cells by segmented filamentous bacteria

open access: yesCell, 2009
SUMMARY The gastrointestinal tract of mammals is inhabited by hundreds of distinct species of commensal microorganisms that exist in a mutualistic relationship with the host. How commensal microbiota influence the host immune system is poorly understood.
I. Ivanov   +16 more
semanticscholar   +1 more source

Human Th17 cells [PDF]

open access: yesArthritis Research & Therapy, 2008
The discovery in mice of a new lineage of CD4+ effector T helper (Th) cells that selectively produce IL-17 has provided exciting new insights into immune regulation, host defence, and the pathogenesis of autoimmune and other chronic inflammatory disorders.
openaire   +2 more sources

The Endogenous Th17 Response in NO2-Promoted Allergic Airway Disease Is Dispensable for Airway Hyperresponsiveness and Distinct from Th17 Adoptive Transfer [PDF]

open access: yes, 2013
Severe, glucocorticoid-resistant asthma comprises 5-7% of patients with asthma. IL-17 is a biomarker of severe asthma, and the adoptive transfer of Th17 cells in mice is sufficient to induce glucocorticoid-resistant allergic airway disease.
Suratt, Benjamin T.   +45 more
core   +1 more source

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