Mast Cells Mediate Rheumatoid Arthritis-Inhibitory Role of IL-37

Pio Conti, Dorina Lauritano, Alessandro Caraffa, Carla E. Gallenga, Francesco Carinci, Gianpaolo Ronconi, Spiros K. Kritas, Paolo Di Emidio, Stefano Martinotti, Franco Pandolfi

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

Rheumatoid arthritis (RA) is an autoimmune, chronic inflammatory, disabling arthropathy that severely affects the quality of life. This disease involves several proinflammatory cytokines, including interleukin (IL)-1 beta and tumor necrosis factor (TNF). IL-1 induces TNF and vice versa, causing joint damage and cartilage degradation. Current antirheumatic drugs may be effective, but they possess many unwanted side effects. In recent years, inhibitors of proinflammatory cytokines have increasingly entered mainstream clinical practice. Recent evidence indicates that IL-37, which has anti-inflammatory properties, is increased in the serum and is released from white blood cells in patients with RA. Mast cells (MCs), stimulated by the neuropeptide substance P (SP) and IL-33, release IL-1 beta and TNF. Recent evidence indicates that large amounts of IL-1 beta and TNF can be released from human MCs, which also secrete CXCL8, which promotes migration of immune cells, causing erosion of the bone and cartilage. Treatment with IL-37 can block the MC stimulation and release of inflammatory compounds, attenuating the severity of the disease and/or altering its progression.
Original languageEnglish
Pages (from-to)267-274
Number of pages8
JournalCritical Reviews in Immunology
Volume39
DOIs
Publication statusPublished - 2019

Keywords

  • IL-37
  • immunity
  • inflammation
  • inhibition
  • mast cell
  • rheumatoid arthritis

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