Elevations in T-helper-2-initiating cytokines (interleukin-33, interleukin-25 and thymic stromal lymphopoietin) in lesional skin from chronic spontaneous (‘idiopathic’) urticaria

2015 ◽  
Vol 172 (5) ◽  
pp. 1294-1302 ◽  
Author(s):  
A.B. Kay ◽  
P. Clark ◽  
M. Maurer ◽  
S. Ying
Keyword(s):  
Thymic Stromal Lymphopoietin ◽  
T Helper ◽  
Lesional Skin ◽  
Interleukin 33 ◽  
T Helper 2 ◽  
Interleukin 25

scholarly journals The Interleukin-33-p38 Kinase Axis Confers Memory T Helper 2 Cell Pathogenicity in the Airway

Immunity ◽  
2015 ◽  
Vol 42 (2) ◽  
pp. 294-308 ◽  
Author(s):  
Yusuke Endo ◽  
Kiyoshi Hirahara ◽  
Tomohisa Iinuma ◽  
Kenta Shinoda ◽  
Damon J. Tumes ◽  
...  
Keyword(s):  
T Helper ◽  
P38 Kinase ◽  
Interleukin 33 ◽  
T Helper 2

scholarly journals NUCLEAR FUNCTION AND RELEASE OF IL-33

2014 ◽  
Vol 21 (03) ◽  
pp. 503-508
Author(s):  
Mousa Komai- Koma
Keyword(s):  
Signal Sequence ◽  
Cellular Interaction ◽  
Cell Phenotype ◽  
Nuclear Factor ◽  
T Helper ◽  
High Endothelial Venules ◽  
Interleukin 33 ◽  
T Helper 2 ◽  
St2 Receptor ◽  
Specific Ligand

Interleukin-33 (IL-33) is the most attractive novel cytokine identified as an IL-1family member. IL-33 was first named NF-HEV (nuclear factor from high endothelial venules), as itwas known to interact with nuclear chromatin although its exact intracellular functions are still tobe clarified. IL-33 is now recognized as the specific ligand for the orphan IL-1 receptor familymember ST2 and to be involved in polarization of T cells towards T helper 2-cell phenotype and inactivation of mast cells, basophils, eosinophils and natural killer cells. It is essential for IL-33 to beextracellularly released in order to bind to the ST2 receptor and consequently play a crucial role ininflammatory, infectious and autoimmune diseases. However, like the IL-1 family members, IL-1beta and IL-18, IL-33 mRNA is translated without a signal sequence for secretion. Additionally, IL-33 cannot be released by the processing and secretion mechanism shared by IL-1beta and IL-18as IL-33 is not a substrate of caspase-1 and does not require proteolysis for activation. In contrast,IL-33 can be inactivated by apoptotic caspases. Accordingly, IL-33 is proposed to be released asan alarmin from necrotic cells but deleted during apoptosis. Besides the known autocrine,paracrine mechanisms of cellular interaction with cytokines, release by necrotic cells is anotherpathway for a cytokine to display its function, which we suggest might be called 'necrocrine'.

Interleukin-25 is involved in cutaneous T-cell lymphoma progression by establishing a T helper 2-dominant microenvironment

2018 ◽  
Vol 178 (6) ◽  
pp. 1373-1382 ◽  
Author(s):  
R. Nakajima ◽  
T. Miyagaki ◽  
M. Hirakawa ◽  
T. Oka ◽  
N. Takahashi ◽  
...  
Keyword(s):  
T Cell ◽  
Cell Lymphoma ◽  
T Cell Lymphoma ◽  
Cutaneous T Cell Lymphoma ◽  
T Helper ◽  
T Helper 2 ◽  
Interleukin 25

Mast cells produce interleukin-25 upon FcεRI-mediated activation

Blood ◽  
2003 ◽  
Vol 101 (9) ◽  
pp. 3594-3596 ◽  
Author(s):  
Kei Ikeda ◽  
Hiroshi Nakajima ◽  
Kotaro Suzuki ◽  
Shin-ichiro Kagami ◽  
Koichi Hirose ◽  
...  
Keyword(s):  
Mast Cells ◽  
Immunoglobulin E ◽  
Th2 Cells ◽  
Cross Linking ◽  
Dependent Manner ◽  
T Helper ◽  
T Helper 2 ◽  
Protein Levels ◽  
Th2 Cell ◽  
Interleukin 25

Interleukin-25 (IL-25) is a recently described T helper 2 (TH2) cell–derived cytokine that belongs to the IL-17 family and induces the production of IL-4, IL-5, and IL-13 from an unidentified non–T-cell population. Here, we show that mast cells are also potent IL-25–producing cells. When bone marrow–derived mast cells were stimulated by immunoglobulin E cross-linking, IL-25 mRNA was induced within 30 minutes in a calcineurin-dependent manner, and the levels of IL-25 mRNA were comparable with those of activated TH2 cells. Production of IL-25 by mast cells was also detected at protein levels by immunoblotting. These results suggest that mast cells may enhance TH2-type immune response by producing IL-25.

scholarly journals The Role of IL-33/ST2 Pathway in Tumorigenesis

2018 ◽  
Vol 19 (9) ◽  
pp. 2676 ◽  
Author(s):  
Kristen Larsen ◽  
Maydelis Minaya ◽  
Vivek Vaish ◽  
Maria Peña
Keyword(s):  
Tumor Regression ◽  
Tumor Development ◽  
Tumor Stroma ◽  
Target Cells ◽  
Dual Function ◽  
T Helper ◽  
Interleukin 33 ◽  
T Helper 2 ◽  
Th2 Immune Response

Cancer is initiated by mutations in critical regulatory genes; however, its progression to malignancy is aided by non-neoplastic cells and molecules that create a permissive environment known as the tumor stroma or microenvironment (TME). Interleukin 33 (IL-33) is a dual function cytokine that also acts as a nuclear factor. IL-33 typically resides in the nucleus of the cells where it is expressed. However, upon tissue damage, necrosis, or injury, it is quickly released into extracellular space where it binds to its cognate receptor suppression of tumorigenicity 2 (ST2)L found on the membrane of target cells to potently activate a T Helper 2 (Th2) immune response, thus, it is classified as an alarmin. While its role in immunity and immune-related disorders has been extensively studied, its role in tumorigenesis is only beginning to be elucidated and has revealed opposing roles in tumor development. The IL-33/ST2 axis is emerging as a potent modulator of the TME. By recruiting a cohort of immune cells, it can remodel the TME to promote malignancy or impose tumor regression. Here, we review its multiple functions in various cancers to better understand its potential as a therapeutic target to block tumor progression or as adjuvant therapy to enhance the efficacy of anticancer immunotherapies.

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