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

Keisuke Oboki, Tatsukuni Ohno, Naoki Kajiwara, Ken Arae, Hideaki Morita, Akina Ishii, Aya Nambu, Takaya Abe, Hiroshi Kiyonari, Kenji Matsumoto, Katsuko Sudo, Ko Okumura, Hirohisa Saito, Susumu Nakae and Charles A. Dinarello
Proceedings of the National Academy of Sciences of the United States of America
Vol. 107, No. 43 (October 26, 2010), pp. 18581-18586
Stable URL: http://www.jstor.org/stable/25748532
Page Count: 6
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IL-33 is a crucial amplifier of innate rather than acquired immunity
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Abstract

IL-33, a member of the IL-1-related cytokines, is considered to be a proallergic cytokine that is especially involved in Th2-type immune responses. Moreover, like IL-1α, IL-33 has been suggested to act as an “alarmin” that amplifies immune responses during tissue injury. In contrast to IL-1, however, the precise roles of IL-33 in those settings are poorly understood. Using IL-1- and IL-33-deficient mice, we found that IL-1, but not IL-33, played a substantial role in induction of T cell-mediated type IV hypersensitivity such as contact and delayed-type hypersensitivity and autoimmune diseases such as experimental autoimmune encephalomyelitis. Most notably, however, IL-33 was important for innate-type mucosal immunity in the lungs and gut. That is, IL-33 was essential for manifestation of T cell-independent protease allergen-induced airway inflammation as well as OVA-induced allergic topical airway inflammation, without affecting acquisition of antigen-specific memory T cells. IL-33 was significantly involved in the development of dextran-induced colitis accompanied by T cell-independent epithelial cell damage, but not in streptozocin-induced diabetes or Con A-induced hepatitis characterized by T cell-mediated apoptotic tissue destruction. In addition, IL-33-deficient mice showed a substantially diminished LPS-induced systemic inflammatory response. These observations indicate that IL-33 is a crucial amplifier of mucosal and systemic innate, rather than acquired, immune responses.

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