Results 31 to 40 of about 123,738 (330)

Dectin-1 Activation Exacerbates Obesity and Insulin Resistance in the Absence of MyD88 [PDF]

open access: yes, 2017
This work was supported by Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP, grant numbers 11/15682-4, 12/02270-2, 15/18121-4), Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq, Regenera INCT Process Grant 465656/2014-5 ...
Aguiar, Cristhiane Favero   +25 more
core   +5 more sources

2008: A MyD88 O, DC [PDF]

open access: yesImmunity, 2008
In this issue of Immunity, Hou et al. (2008) describe the generation of mice that selectively lack the adaptor protein MyD88 in dendritic cells (DCs). These mice demonstrate that the requirement for Toll-like receptor (TLR) signaling in DCs is dependent on the physical form of the TLR ligand.
Pulendran, Bali, Cao, Weiping
openaire   +2 more sources

Mechanism of MyD88S mediated signal termination [PDF]

open access: yesCell Communication and Signaling, 2022
Abstract Background A universal adaptor protein, MyD88, orchestrates the innate immune response by propagating signals from toll-like receptors (TLRs) and interleukin-1 receptor (IL-1R). Receptor activation seeds MyD88 dependent formation of a signal amplifying supramolecular organizing center (SMOC)—the myddosome ...
Katarzyna Pustelny   +9 more
openaire   +4 more sources

Drug-like analogues of the parasitic worm-derived immunomodulator ES-62 are therapeutic in the MRL/Lpr model of systemic lupus erythematosus [PDF]

open access: yes, 2015
Introduction ES-62, a phosphorylcholine (PC)-containing immunomodulator secreted by the parasitic worm Acanthocheilonema viteae, protects against nephritis in the MRL/Lpr mouse model of systemic lupus erythematosus (SLE).
Harnett, M. M.   +4 more
core   +1 more source

The parasitic worm-derived immunomodulator, ES-62 and its drug-like small molecule analogues exhibit therapeutic potential in a model of chronic asthma [PDF]

open access: yes, 2016
Chronic asthma is associated with persistent lung inflammation and long-term remodelling of the airways that have proved refractory to conventional treatments such as steroids, despite their efficacy in controlling acute airway contraction and bronchial ...
Al-Riyami, L.   +6 more
core   +1 more source

Mapping the human T cell repertoire to recurrent driver mutations in MYD88 and EZH2 in lymphoma

open access: yesOncoImmunology, 2017
Oncogenic “driver” mutations are theoretically attractive targets for the immunotherapy of lymphoid cancers, yet the proportion that can be recognized by T cells remains poorly defined. To address this issue without any confounding effects of the patient'
Julie S. Nielsen   +17 more
doaj   +1 more source

Overexpression of the toll-like receptor (TLR) signaling adaptor MYD88, but lack of genetic mutation, in myelodysplastic syndromes. [PDF]

open access: yesPLoS ONE, 2013
MYD88 is a key mediator of Toll-like receptor innate immunity signaling. Oncogenically active MYD88 mutations have recently been reported in lymphoid malignancies, but has not been described in MDS.
Sophie Dimicoli   +13 more
doaj   +1 more source

MyD88-dependent interplay between myeloid and endothelial cells in the initiation and progression of obesity-associated inflammatory diseases. [PDF]

open access: yes, 2014
Low-grade systemic inflammation is often associated with metabolic syndrome, which plays a critical role in the development of the obesity-associated inflammatory diseases, including insulin resistance and atherosclerosis.
DeFranco, Anthony L   +19 more
core   +2 more sources

Hematopoietic but not endothelial cell MyD88 contributes to host defense during gram-negative pneumonia derived sepsis. [PDF]

open access: yesPLoS Pathogens, 2014
Klebsiella pneumoniae is an important cause of sepsis. The common Toll-like receptor adapter myeloid differentiation primary response gene (MyD)88 is crucial for host defense against Klebsiella.
Miriam H P van Lieshout   +6 more
doaj   +1 more source

Ischemia and reperfusion injury in kidney transplantation : relevant mechanisms in injury and repair [PDF]

open access: yes, 2020
Ischemia and reperfusion injury (IRI) is a complex pathophysiological phenomenon, inevitable in kidney transplantation and one of the most important mechanisms for non- or delayed function immediately after transplantation.
Berger, Stefan P.   +7 more
core   +2 more sources

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