Pathophysiologic role of Interleukin-33/ST2 in Sjögren's syndrome

Soyfoo, Muhammad Shahnawaz; Nicaise, Charles

doi:10.1016/j.autrev.2021.102756

Cited by 23 publications

(19 citation statements)

References 89 publications

(110 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…IL-33 is also a member of the IL-1 family and has dual functions as a nuclear factor and a cytokine. In SS patients, the serum level of IL-33 is significantly increased to promote IFN-γ and inflammation, which in turn increases the activation of the IL-33/ST2 pathway, leading to worsening of the disease [53]. IL-2 and IL-21 belong to the IL-2 family.…”

Section: Cytokinesmentioning

confidence: 99%

Advances in Pathogenesis of Sjögren’s Syndrome

Tian

Yang

Liu

et al. 2021

Journal of Immunology Research

View full text Add to dashboard Cite

Sjögren’s syndrome (SS) is a chronic autoimmune disease of unknown etiology that mainly involves exocrine glands. Patients present with dry mouth and eyes, fever, arthralgia, and other systemic symptoms. In severe cases, the quality of life of patients is affected. At present, there is no cure for SS, and the treatment options are extremely limited. In recent years, studies of patients and animal models have identified abnormalities of immune cell function and cytokines to be involved in SS. A systematic review of the literature may clarify the etiology and pathogenesis of SS, as well as provide a theoretical basis for the development of new drugs for the treatment of SS.

show abstract

Section: Cytokinesmentioning

confidence: 99%

Advances in Pathogenesis of Sjögren’s Syndrome

Tian

Yang

Liu

et al. 2021

Journal of Immunology Research

View full text Add to dashboard Cite

show abstract

“…Rheumatic diseases are immune-mediated chronic inflammatory syndromes, which are characterized by the hyperactivity of effector Th1 cells and Th17 cells, dysfunction of Tregs, activation of autoreactive B cells, and production of autoantibodies ( 58 ). A growing number of studies have found that the level of IL-33 is associated with the severity of rheumatic disease, indicating that IL-33 and ST2 may be potential targets for predicting the development of disease and improving the clinical outcomes ( 59 , 60 ). Next, we will discuss the role of the IL-33/ST2 axis in several common rheumatic diseases ( Table 1 , Figure 5 ).…”

Section: Il-33/st2 Axis In Rheumatic Diseasesmentioning

confidence: 99%

“…But when combined with IL-12 and/or IL-23, it promoted the release of IFN-γ by up to 10 times in NK and NKT cells. Moreover, TNF-α, IL-1β, and IFN-γ in the inflammatory environment could further increase the activation of IL-33, forming positive feedback ( 60 ). Therefore, the targeting IL-33/ST2 axis may be a promising treatment option for pSS.…”

Section: Il-33/st2 Axis In Rheumatic Diseasesmentioning

confidence: 99%

IL-33 in Rheumatic Diseases

2021

View full text Add to dashboard Cite

Interleukin-33 (IL-33) is a nuclear factor mainly expressed in barrier epithelium, endothelial cells, and fibroblast reticular cells. Some inflammatory cells also express IL-33 under certain conditions. The important role of IL-33 in allergic reactions, helminth infection, cancer, tissue fibrosis, chronic inflammation, organ transplantation, and rheumatic immune diseases has been extensively studied in recent years. IL-33 primarily activates various circulating and tissue-resident immune cells, including mast cell, group 2 innate lymphoid cell (ILC2), regulatory T cell (Treg), T helper 2 cell (Th2), natural killer cell (NK cell), and macrophage. Therefore, IL-33 plays an immunomodulatory role and shows pleiotropic activity in different immune microenvironments. The IL-33/serum stimulation-2 (ST2) axis has been shown to have a detrimental effect on rheumatoid arthritis, systemic lupus erythematosus, and other rheumatic diseases. Interestingly, IL-33 also plays a protective role in the repair of barrier epithelium and the activation of Tregs. Therefore, the role of IL-33/ST2 depends on the underlying pathological conditions in rheumatic diseases. This review focuses on the dual role of the IL-33/ST2 axis in rheumatic diseases.

show abstract

“…The subsequent activation of plasmacytoid dendritic cells (pDC) triggers a massive release of IFN-α and the release of B cell activating factor (BAFF) that support the proliferation of B cells inside germinal centers (GC). IFN-γ in turn acts on the salivary gland epithelial cells (SGEC) to further release alarmins in the extracellular milieu, thereby constituting a vicious auto-inflammatory loop fostering local and systemic damage and contributing to disease perpetuation [ 12 ].…”

Section: Introductionmentioning

confidence: 99%

The Involvement of Alarmins in the Pathogenesis of Sjögren’s Syndrome

Sarrand

Baglione

Parisis

et al. 2022

IJMS

View full text Add to dashboard Cite

Sjogren’s syndrome (SS) is a chronic autoimmune disease that affects exocrine glands, primarily the salivary and lachrymal glands. It is characterized by lymphoplasmacytic infiltration of the glandular tissues, ultimately leading to their dysfunction and destruction. Besides classic dry eyes and dry mouth defined as sicca syndrome, patients affected by the disease also typically display symptoms such as fatigue, pain and in more than 50% of cases, systemic manifestations such as arthritis, interstitial lung involvement, neurological involvement and an increased risk of lymphoma. The pathophysiological mechanisms underlying SS still remain elusive. The crucial role of innate immunity has been advocated in recent years regarding the pathogenesis of pSS, especially in the initiation and progression toward autoimmunity. Alarmins are endogenous molecules that belong to the large family of damage associated molecular pattern (DAMP). Alarmins are rapidly released, ensuing cell injury and interacting with pattern recognition receptors (PRR) such as toll-like receptors (TLR) to recruit and activate cells of the innate immune system and to promote adaptive immunity responses. This review highlights the current knowledge of various alarmins and their role in the pathogenesis of pSS.

show abstract

Pathophysiologic role of Interleukin-33/ST2 in Sjögren's syndrome

Cited by 23 publications

References 89 publications

Advances in Pathogenesis of Sjögren’s Syndrome

Advances in Pathogenesis of Sjögren’s Syndrome

IL-33 in Rheumatic Diseases

The Involvement of Alarmins in the Pathogenesis of Sjögren’s Syndrome

Contact Info

Product

Resources

About