期刊
EXPERT OPINION ON THERAPEUTIC TARGETS
卷 21, 期 12, 页码 1141-1152出版社
TAYLOR & FRANCIS LTD
DOI: 10.1080/14728222.2017.1398734
关键词
Allodynia; glial cells; inflammatory pain; hyperalgesia; MAPK; neuropathy; nociceptors; pain therapy; sensory neurons
资金
- PPSUS - CNPq
- Fundacao Araucaria
- SESA-PR
- FAPESP (Fundacao de Amparo a Pesquisa do Estado de Sao Paulo) [2011/19670-0, 2013/08216-2]
- CAPES
- CNPq
- MCTI/FINEP/CT-INFRA-PROINFRA [02/2014, 0119/16, 01.12.0294.00, 01.13.0049.00]
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.
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