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

K Oboki, T Ohno, N Kajiwara, K Arae… - Proceedings of the …, 2010 - National Acad Sciences
K Oboki, T Ohno, N Kajiwara, K Arae, H Morita, A Ishii, A Nambu, T Abe, H Kiyonari…
Proceedings of the National Academy of Sciences, 2010National Acad Sciences
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 …
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.
National Acad Sciences