Targeting IL-33/ST2 signaling: regulation of immune function and analgesia

Autor(es)

Fattori, Victor ^[1] ; Hohmann, Miriam S. N. ^[1] ; Rossaneis, Ana C. ^[1] ; Manchope, Marilia F. ^[1] ; Alves-Filho, Jose C. ^[2] ; Cunha, Thiago M. ^[2] ; Cunha, Fernando Q. ^[2] ; Verri, Jr., Waldiceu A. ^[1]

Afiliação do(s) autor(es)

^[1] Univ Estadual Londrina, Ctr Ciencias Biol, Dept Ciencias Patol, Londrina - Brazil

^[2] Univ Sao Paulo, Ribeirao Preto Med Sch, Dept Pharmacol, Ribeirao Preto - Brazil

• Tipo de documento: Artigo de Revisão
• Fonte: EXPERT OPINION ON THERAPEUTIC TARGETS; v. 21, n. 12, p. 1141-1152, 2017.
• Citações Web of Science: 13

Resumo

Introduction: IL-33 signals through ST2 receptor and promotes inflammation by activating downstream pathways culminating in the production of pro-inflammatory mediators such as IL-1, TNF-, and IL-6 in an NF-B-dependent manner. In fact, compelling evidence has demonstrated the importance of IL-33/ST2 in both innate and adaptive immune responses in diseases presenting pain as an important clinical symptom.Areas covered: IL-33 is a pleiotropic cytokine with varied immune functions. Dysregulation of this pathway has been described as a key step in varied immune responses. Further, IL-33 contributes to peripheral and spinal cord nociceptor neuron sensitization in innate and adaptive inflammatory immune responses as well as in neuropathic and cancer pain. In this sense, targeting IL-33/ST2 signaling is a promising therapeutic approach.Expert opinion: The modulation of IL-33/ST2 signaling represents a possible approach in regulating immune functions. In addition to immune function, strategies targeting IL-33/ST2 signaling pathway display a favorable preclinical analgesic profile in both acute and chronic models of pain. Therefore, IL-33-targeting therapies represent a potential target for the development of novel analgesic drugs given that IL-33 activates, for instance, neutrophils, mast cells, macrophages, astrocytes, and microglia that are important cells in the induction and maintenance of chronic pain states. (AU)

• Processo FAPESP: 13/08216-2 - CPDI - Centro de Pesquisa em Doenças Inflamatórias
• Beneficiário: Fernando de Queiroz Cunha
• Modalidade de apoio: Auxílio à Pesquisa - Centros de Pesquisa, Inovação e Difusão - CEPIDs
• Processo FAPESP: 11/19670-0 - Mecanismos envolvidos na fisiopatologia da artrite reumatóide, dor e sepse
• Beneficiário: Fernando de Queiroz Cunha
• Modalidade de apoio: Auxílio à Pesquisa - Temático