| Full text | |
| Author(s): |
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]
Total Authors: 8
|
| Affiliation: | [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
Total Affiliations: 2
|
| Document type: | Review article |
| Source: | EXPERT OPINION ON THERAPEUTIC TARGETS; v. 21, n. 12, p. 1141-1152, 2017. |
| Web of Science Citations: | 13 |
| Abstract | |
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) | |
| FAPESP's process: | 13/08216-2 - CRID - Center for Research in Inflammatory Diseases |
| Grantee: | Fernando de Queiroz Cunha |
| Support Opportunities: | Research Grants - Research, Innovation and Dissemination Centers - RIDC |
| FAPESP's process: | 11/19670-0 - Mechanisms involved in the pathophysiology of rheumatoid arthritis, pain and sepsis |
| Grantee: | Fernando de Queiroz Cunha |
| Support Opportunities: | Research Projects - Thematic Grants |