Results 21 to 30 of about 67,088,256 (273)

IL-33 and IL-33 Receptors in Host Defense and Diseases

open access: yesAllergology International, 2010
Interleukin-33 (IL-33) is a member of the IL-1 cytokine family, which includes IL-1 and IL-18. IL-33 is considered to be crucial for induction of Th2-type cytokine-associated immune responses such as host defense against nematodes and allergic diseases by inducing production of such Th2-type cytokines as IL-5 and IL-13 by Th2 cells, mast cells ...
Oboki, Keisuke   +4 more
openaire   +2 more sources

Lung epithelium is the major source of IL-33 and is regulated by IL-33-dependent and IL-33-independent mechanisms in pulmonary cryptococcosis [PDF]

open access: yesPathogens and Disease, 2016
Inhalation of the fungus Cryptococcus neoformans (C. neoformans) results in pulmonary cryptococcosis associated with IL-33-dependent type 2 immunity. Lung epithelium represents the initial contact site of infection. The role of IL-33 in type 2 immunity has been analyzed, but the source of this cytokine and its effect on lung epithelial cell function in
Laura, Heyen   +6 more
openaire   +2 more sources

IL-33 biology in cancer: An update and future perspectives. [PDF]

open access: yes, 2022
Interleukin-33 (IL-33) is a member of the IL-1 family of cytokines that is constitutively expressed in the nucleus of epithelial, endothelial and fibroblast-like cells.
Vu, Vivian P   +5 more
core   +2 more sources

IL-33 Supplemental

open access: yes, 2023
IL-33 Supplemental ...
Xi Wang (13171239)
core   +1 more source

Serum IL-33 level and IL-33 gene polymorphisms in Behçet’s disease

open access: yesRheumatology International, 2014
Behçet's disease (BD) is a chronic inflammatory disease. Increased productions of cytokines including interleukin (IL)-1β and IL-18 are documented, and IL-1α and β gene polymorphisms are associated with susceptibility to the disease. IL-33 is a recently discovered member of IL-1 cytokine family.
Koca S.S.   +6 more
openaire   +2 more sources

IL-33-Induced Cytokine Secretion and Survival of Mouse Eosinophils Is Promoted by Autocrine GM-CSF. [PDF]

open access: yes, 2016
Eosinophils are major effector cells during allergic responses and helminth infections. Recent studies further highlight eosinophils as important players in many other biological processes.
David Voehringer (713702)   +5 more
core   +2 more sources

The association between airway eosinophilic inflammation and IL-33 in stable non-atopic COPD

open access: yesRespiratory Research, 2018
Background Interleukin(IL)-33 is an epithelial alarmin important for eosinophil maturation, activation and survival. The aim of this study was to examine the association between IL-33, its receptor expression and airway eosinophilic inflammation in non ...
Damian Tworek   +8 more
doaj   +1 more source

DataSheet_1_Rapamycin Dampens Inflammatory Properties of Bone Marrow ILC2s in IL-33-Induced Eosinophilic Airway Inflammation.docx

open access: yes, 2022
The alarmin cytokine interleukin (IL)-33 plays an important proinflammatory role in type 2 immunity and can act on type 2 innate lymphoid cells (ILC2s) and type 2 T helper (TH2) cells in eosinophilic inflammation and asthma.
Julie Weidner (3994631)   +5 more
core   +1 more source

IL-33 Signaling in Lung Injury [PDF]

open access: yesTranslational Perioperative and Pain Medicine, 2016
Interleukin (IL)-33, a member of the IL-1 cytokine super-family, acts as both a traditional cytokine and an intracellular nuclear factor. It is generally released from damaged immune cells and signals through its receptor ST2 in an autocrine and paracrine fashion, plays important roles in type-2 innate immunity, and functions as an "alarmin" or a ...
Jing, Chang   +3 more
openaire   +2 more sources

Structural Basis of IL-1 Family Cytokine Signaling

open access: yesFrontiers in Immunology, 2019
Interleukin-1 (IL-1) family cytokines are key signaling molecules in both the innate and adaptive immune systems, mediating inflammation in response to a wide range of stimuli.
James K. Fields   +6 more
doaj   +1 more source

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