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Role of interleukin 33 in respiratory allergy and asthma

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LANCET RESPIRATORY MEDICINE
卷 2, 期 3, 页码 226-237

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ELSEVIER SCI LTD
DOI: 10.1016/S2213-2600(13)70261-3

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资金

  1. ERC [233015]
  2. Clinical Chair from Asthma UK [CH11SJ]
  3. MRC Centre Grant [G1000758]
  4. Predicta FP7 Collaborative Project grant [260895]
  5. Wellcome Trust
  6. Rosetrees Trust
  7. BMA
  8. EAACI
  9. ERS
  10. MRC [G1000758] Funding Source: UKRI
  11. European Research Council (ERC) [233015] Funding Source: European Research Council (ERC)
  12. Asthma UK [MRC-AsthmaUKCentre] Funding Source: researchfish
  13. Medical Research Council [G1000758] Funding Source: researchfish

向作者/读者索取更多资源

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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