IL-33 in Rheumatic Diseases

Dong, Yuanji; Zhong, Jixin; Dong, Lingli

doi:10.3389/fmed.2021.739489

Cited by 25 publications

(20 citation statements)

References 125 publications

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“…IL-33 is a nuclear factor expressed in the nuclei of structural cells and innate cells, which is released upon cell damage and necrosis ( 39 ). Once released, IL-33 propagates Th2 immune responses by activating ILC2s, Th2 cells, DCs, eosinophils, mast cells, and basophils.…”

Section: Induction Phasementioning

confidence: 99%

“…IL-33 signals through the heterodimeric complex consisting of interleukin-1 receptor-like 1 (IL1RL1 or ST2) and IL-1R accessory protein (IL-1RAcP). Due to its strong induction of type 2 responses, IL-33 is a central player in driving allergic disease ( 39 ). However, IL-33 is also involved in maintaining tissue homeostasis and tissue repair via activating ST2 + regulatory T (Treg) cells and ILC2s to produce amphiregulin (Areg) ( 41 ).…”

Section: Induction Phasementioning

confidence: 99%

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T Helper 2-Associated Immunity in the Pathogenesis of Systemic Lupus Erythematosus

Kim

2022

Front. Immunol.

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Systemic Lupus Erythematosus (SLE) is a chronic autoimmune disease that mainly affects women in their reproductive years. A complex interaction of environmental and genetic factors leads to the disruption of immune tolerance towards self, causing overt immune activation and production of autoantibodies that attack multiple organs. Kidney damage, termed lupus nephritis, is the leading cause of SLE-related morbidity and mortality. Autoantibodies are central to propagating lupus nephritis through forming immune complexes and triggering complements. Immunoglobulin G (IgG) potently activates complement; therefore, autoantibodies were mainly considered to be of the IgG isotype. However, studies revealed that over 50% of patients produce autoantibodies of the IgE isotype. IgE autoantibodies actively participate in disease pathogenesis as omalizumab treatment, a humanized anti-IgE monoclonal antibody, improved disease severity in an SLE clinical trial. IgE is a hallmark of T helper 2-associated immunity. Thus, T helper 2-associated immunity seems to play a pathogenic role in a subset of SLE patients. This review summarizes human and animal studies that illustrate type 2 immune responses involved during the pathology of SLE.

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Section: Induction Phasementioning

confidence: 99%

Section: Induction Phasementioning

confidence: 99%

T Helper 2-Associated Immunity in the Pathogenesis of Systemic Lupus Erythematosus

Kim

2022

Front. Immunol.

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“…Thus, IL-33 plays a major role in the initiation and development of type 2 immune responses, which are essential during host infection by helminths for example [ 27 , 111 , 112 ], but which, on the other hand, contribute to the development of various allergic diseases, such as asthma or atopic dermatitis. The precise role of IL-33 in these pathologies and its mechanism of action have been widely described in various reviews [ 90 , 91 , 96 , 113 , 114 , 115 , 116 , 117 ]. Importantly, IL-33 plays a major role in human asthma, since the IL33 and IL1RL1 genes have been identified, on a recurrent basis, as susceptibility genes for asthma in very large genetic studies [ 118 , 119 ] (for reviews, see [ 17 , 120 , 121 ]).…”

Section: The Il-33/st2l Axis: From Discovery To Functionmentioning

confidence: 99%

“…Given the many functions of IL-33, it is not surprising that it is associated with many diseases and the subject has already been extensively covered by various reviews [ 90 , 91 , 96 ]. In addition to the allergic diseases mentioned above, IL-33 is associated with many chronic inflammatory and/or fibrotic pathologies affecting various organs, such as the intestine in the case of ulcerative colitis or the lung in the case of COPD [ 113 , 114 , 116 ]. It is also involved in infectious diseases (sepsis, infection by worms, viruses or bacteria), cardiovascular diseases (atherosclerosis), renal diseases, metabolic diseases and in tumors, having either a protective or a detrimental role in these pathologies [ 90 , 91 , 96 , 149 ].…”

Section: The Il-33/st2l Axis: From Discovery To Functionmentioning

confidence: 99%

IL-33, an Alarmin of the IL-1 Family Involved in Allergic and Non Allergic Inflammation: Focus on the Mechanisms of Regulation of Its Activity

Cayrol

2021

Cells

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Interleukin-33 (IL-33) is a member of the interleukin-1 (IL-1) family that is expressed in the nuclei of endothelial and epithelial cells of barrier tissues, among others. It functions as an alarm signal that is released upon tissue or cellular injury. IL-33 plays a central role in the initiation and amplification of type 2 innate immune responses and allergic inflammation by activating various target cells expressing its ST2 receptor, including mast cells and type 2 innate lymphoid cells. Depending on the tissue environment, IL-33 plays a wide variety of roles in parasitic and viral host defense, tissue repair and homeostasis. IL-33 has evolved a variety of sophisticated regulatory mechanisms to control its activity, including nuclear sequestration and proteolytic processing. It is involved in many diseases, including allergic, inflammatory and infectious diseases, and is a promising therapeutic target for the treatment of severe asthma. In this review, I will summarize the literature around this fascinating pleiotropic cytokine. In the first part, I will describe the basics of IL-33, from the discovery of interleukin-33 to its function, including its expression, release and signaling pathway. The second part will be devoted to the regulation of IL-33 protein leading to its activation or inactivation.

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“…IL-33 is one of the most recently discovered member of the IL-1 cytokine family (6)(7)(8)(9), while IL-13 is a prototypical Th2 cytokine (10)(11)(12). Recent evidence show that the Th2 cytokines IL-4 and IL-13 are higher in SSc patients and promote fibrotic responses (12)(13)(14).…”

Section: Introductionmentioning

confidence: 99%

IL-13 and IL-33 Serum Levels Are Increased in Systemic Sclerosis Patients With Interstitial Lung Disease

et al. 2022

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ObjectiveSystemic sclerosis (SSc) mortality is extremely variable in its internal organ involvement. Pulmonary fibrosis occurs in up to 30% of the cases. Animal models provide evidence that IL-33 is able to induce both cutaneous and pulmonary fibrosis via increased IL-13 and in SSc patients the levels of IL-33 correlate with skin fibrosis. Our aim was to test whether both IL-33 and IL-13 are higher in patients with diffuse SSc and interstitial lung disease (SSc-ILD) compared to SSc patients without ILD and healthy controls.MethodsSerum levels of IL-13 and IL-33 were measured in 30 SSc patients with diffuse disease and 30 healthy controls by enzyme-linked immunosorbent assay. The extent of pulmonary fibrosis was assessed according to HRCT Warrick score. Pulmonary function tests included lung diffusion capacity for carbon monoxide, forced vital capacity and total lung capacity.ResultsBoth IL-13 and IL-33 levels were increased in SSc patients compared to controls and significantly associated each other. DLco, FVC and TLC scores were inversely associated with IL-33 and IL-13 levels. Both IL-33 and IL-13 levels were significantly associated with the Warrick severity score and higher in the group of SSc patients with reduced pulmonary function compared to SSc patients with normal pulmonary function tests.ConclusionThe IL-13/IL-33 axis needs to be further explored in longitudinal studies of SSc-ILD patients to assess its validity as a biomarker and future treatment target, as does downstream mediator ST2.

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IL-33 in Rheumatic Diseases

Cited by 25 publications

References 125 publications

T Helper 2-Associated Immunity in the Pathogenesis of Systemic Lupus Erythematosus

T Helper 2-Associated Immunity in the Pathogenesis of Systemic Lupus Erythematosus

IL-33, an Alarmin of the IL-1 Family Involved in Allergic and Non Allergic Inflammation: Focus on the Mechanisms of Regulation of Its Activity

IL-13 and IL-33 Serum Levels Are Increased in Systemic Sclerosis Patients With Interstitial Lung Disease

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