Semantic Scholar Open Access 2019 134 sitasi

IL-33/IL-31 Axis in Immune-Mediated and Allergic Diseases

G. Murdaca M. Greco A. Tonacci S. Negrini M. Borro +2 lainnya

Abstrak

Several allergic and immunologic diseases including asthma, food allergy (FA), chronic spontaneous urticaria (CSU), atopic dermatitis (AD), systemic lupus erythematosus (SLE), systemic sclerosis (SSc), rheumatoid arthritis (RA), and Behçet’s disease (BD) are characterized by the involvement of Th2 immunity. Several mediators lead to immunoglobulin (Ig)E production, thus including key cytokines such as interleukin (IL)-4, IL-5, and IL-13. Among them, IL-31 and IL-33 have been recently studied as novel biomarkers and future therapeutic targets for allergic and immunological disorders. IL-31 is a proinflammatory cytokine—it regulates cell proliferation and is involved in tissue remodeling. IL-33, acting through its receptor suppression of tumorigenity (ST2L), is an alarmin cytokine from the IL-1 family, whose expression is mediated by tissue damage. The latter has a pleiotropic effect, as it may modulate specific and innate immune cells functions. To date, several researchers have investigated the involvement of IL-31 and IL-33 in several allergic and immune-mediated diseases. Further studies are needed to understand the future applications of these molecules as novel therapeutic agents. This paper aims to give the readers a complete and updated review of IL-31 and IL-33 involvement among the most common autoimmune and allergic disorders.

Topik & Kata Kunci

Penulis (7)

G

G. Murdaca

M

M. Greco

A

A. Tonacci

S

S. Negrini

M

M. Borro

F

F. Puppo

S

S. Gangemi

Format Sitasi

Murdaca, G., Greco, M., Tonacci, A., Negrini, S., Borro, M., Puppo, F. et al. (2019). IL-33/IL-31 Axis in Immune-Mediated and Allergic Diseases. https://doi.org/10.3390/ijms20235856

Akses Cepat

Lihat di Sumber doi.org/10.3390/ijms20235856
Informasi Jurnal
Tahun Terbit
2019
Bahasa
en
Total Sitasi
134×
Sumber Database
Semantic Scholar
DOI
10.3390/ijms20235856
Akses
Open Access ✓