期刊
LANCET RESPIRATORY MEDICINE
卷 2, 期 3, 页码 226-237出版社
ELSEVIER SCI LTD
DOI: 10.1016/S2213-2600(13)70261-3
关键词
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资金
- ERC [233015]
- Clinical Chair from Asthma UK [CH11SJ]
- MRC Centre Grant [G1000758]
- Predicta FP7 Collaborative Project grant [260895]
- Wellcome Trust
- Rosetrees Trust
- BMA
- EAACI
- ERS
- MRC [G1000758] Funding Source: UKRI
- European Research Council (ERC) [233015] Funding Source: European Research Council (ERC)
- Asthma UK [MRC-AsthmaUKCentre] Funding Source: researchfish
- Medical Research Council [G1000758] Funding Source: researchfish
Since the discovery of interleukin 33 as the adopted ligand for the then orphan ST2 receptor, many studies have implicated this cytokine in the pathogenesis of respiratory allergy and asthma. Although some extracellular functions of interleukin 33 have been well defined, many aspects of the regulation and secretion of this cytokine need clarification. Interleukin 33 has been identified as a trigger of T-helper-type-2 cell differentiation, which by interacting with both the innate and the adaptive immune systems, can drive allergy and asthma pathogenesis. However, induction of interleukin 33 by both environmental and endogenous triggers implies a possible role during infection and tissue damage. Further understanding of the biology of interleukin 33 will clarify its possible role in future therapeutic interventions.
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