IL-33 is a crucial amplifier of innate rather than acquired immunity

By K. Oboki, T. Ohno, Naoki Kajiwara, K. Arae, H. Morita, Akina Ishii, Aya Nambu, T. Abe, H. Kiyonari, Kenji Matsumoto and 4 more. Proceedings of the National Academy of Sciences of the United States of America, 2010

650 citations recorded by the source corpus.

Subfields: Immunology, Surgery

View Paper: https://www.semanticscholar.org/paper/0659abe6e2e9cdc216202830e7aba7c84c5c6172

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Immunology

1. C. Garlanda
2. A. Mantovani
3. C. Cayrol
4. C. A. Dinarello
5. J. Girard
6. F. Powrie
7. A. Sica
8. P. Allavena

In Surgery

1. C. Cayrol
2. J. Girard
3. C. A. Dinarello
4. A. Mantovani
5. C. Garlanda

Citations in the corpus

• THE INTERLEUKIN-1 FAMILY: BACK TO THE FUTURE (2013, positive): “IL-33 amplifies innate immunity and inflammatory responses, not necessarily dependent on the development of adaptive Th2 cell responses (Oboki et al., 2010).”
• Lung natural helper cells are a critical source of Th2 cell-type cytokines in protease allergen-induced airway inflammation. (2012, background): “It also causes asthma-like symptoms in RAG-deficient mice (Oboki et al., 2010).”
• IL-33: an alarmin cytokine with crucial roles in innate immunity, inflammation and allergy. (2014, background): “IL-33 was found to be required for ovalbumininduced and protease allergen (papain)-induced airway inflammation [22,23].”
• Cytokine Networks in the Pathophysiology of Inflammatory Bowel Disease. (2019, background): “Administration of IL-33 aggravates, whereas the blockade of IL-33 or its receptor ST2, suppresses early acute colitis in DSS- and 2,4,6-trinitrobenzenesulfonic acid solution (TNBS)-induced models (Oboki et al., 2010; Sedhom et al., 2013).”