IL-22 Binding Protein Promotes the Disease Process in Multiple Sclerosis

Lindahl, Hannes; Guerreiro-Cacais, André Ortlieb; Bedri, Sahl Khalid; Linnerbauer, Mathias; Lindén, Magdalena; Abdelmagid, Nada; Tandre, Karolina; Hollins, Claire; Irving, Lorraine; Glover, Colin P.; Jones, Clare A.; Alfredsson, Lars; Rönnblom, Lars; Kockum, Ingrid; Khademi, Mohsen; Jagodic, Maja; Olsson, Tomas

doi:10.4049/jimmunol.1900400

Cited by 17 publications

(16 citation statements)

References 37 publications

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“…The severity of inflammation was positively correlated with the level of IL-22BP in the cerebrospinal fluid of patients with MS. IL-22BP has a pathogenic effect on EAE in both mice and rats, and IL-22BP is theoretically an antagonist of IL-22. IL-22BP has been proposed to reduce IFN-γ produced by brain-derived T cells in lymph nodes ( 92 ). Previous studies showed that the histopathological features of EAE in IL-22-deficient mice were comparable to those in wild-type mice ( 14 ).…”

Section: Th22 Cells In Autoimmune Diseasesmentioning

confidence: 99%

“…Previous studies showed that the histopathological features of EAE in IL-22-deficient mice were comparable to those in wild-type mice ( 14 ). Hannes et al conducted EAE experiments on wild-type mice, IL-22 deficient mice, IL-22BP deficient mice, and IL-22 and IL-22BP double deficient mice and concluded that the loss of control of IL-22 signal in IL-22BP deficient mice reduced the severity of EAE,which supported the protective effect of IL-22 in MS; thus, they suggested that IL-22BP could be used as a new target for MS ( 92 ).…”

Section: Th22 Cells In Autoimmune Diseasesmentioning

confidence: 99%

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Role of Th22 Cells in the Pathogenesis of Autoimmune Diseases

et al. 2021

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Upon antigenic stimulation, naïve CD4+T cells differentiate into different subsets and secrete various cytokines to exert biological effects. Th22 cells, a newly identified CD4+T cell subset,are distinct from the Th1, Th2 and Th17 subsets. Th22 cells secrete certain cytokines such as IL-22, IL-13 and TNF-α, but not others, such as IL-17, IL-4, or interferon-γ (IFN-γ), and they express chemokine receptors CCR4, CCR6 and CCR10. Th22 cells were initially found to play a role in skin inflammatory diseases, but recent studies have demonstrated their involvement in the development of various autoimmune diseases. Here, we review research advances in the origin, characteristics and effector mechanisms of Th22 cells, with an emphasis on the role of Th22 cells and their main effector cytokine IL-22 in the pathogenesis of autoimmune diseases. The findings presented here may facilitate the development of new therapeutic strategies for targeting these diseases.

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Section: Th22 Cells In Autoimmune Diseasesmentioning

confidence: 99%

Section: Th22 Cells In Autoimmune Diseasesmentioning

confidence: 99%

Role of Th22 Cells in the Pathogenesis of Autoimmune Diseases

et al. 2021

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“…On the contrary, TGF-β ( 53 ), ICOS ( 54 ), and IL-27 ( 55 ) have also been shown to prevent the production of IL-22. Lastly, IL-22BP is a natural inhibitor of IL-22, having more than a 20-fold higher affinity for IL-22 than the cell surface receptor chain IL-22R1 ( 56 ), thus playing a pathogenic role in inflammatory bowel disease (IBD) ( 57 ) and multiple sclerosis ( 58 ) patients.…”

Section: Regulation Of Il-10 and Il-22 Secretion By Mucosal Immune Cementioning

confidence: 99%

IL-10 and IL-22 in Mucosal Immunity: Driving Protection and Pathology

2020

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The barrier surfaces of the gastrointestinal tract are in constant contact with various microorganisms. Cytokines orchestrate the mucosal adaptive and innate immune cells in the defense against pathogens. IL-10 and IL-22 are the best studied members of the IL-10 family and play essential roles in maintaining mucosal homeostasis. IL-10 serves as an important regulator in preventing pro-inflammatory responses while IL-22 plays a protective role in tissue damage and contributes to pathology in certain settings. In this review, we focus on these two cytokines in the development of gastrointestinal diseases, including inflammatory bowel diseases (IBD) and colitis-associated cancer (CAC). We summarize the recent studies and try to gain a better understanding on how they regulate immune responses to maintain equilibrium under inflammatory conditions.

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“…In a follow-up study the role of IL-22BP in EAE was further dissected using an inducible in vivo IL-22BP knockdown rat strain. Reducing IL-22BP expression before EAE immunization results in reduced incidence and severity of disease in conjunction with increased proportions of Tregs and decreased proportions of Th1 cells in the lymph nodes that drain the site of immunization ( 80 ). Taken together, IL-22 appears to have a protective effect in autoimmune neuroinflammation but, unlike many other animal models discussed in this article, the effect of endogenous IL-22 is normally blocked by IL-22BP.…”

Section: The Influence Of Interleukin-22 On the Th1/th17 Axismentioning

confidence: 99%

Interleukin-22 Influences the Th1/Th17 Axis

Lindahl

Olsson

2021

Front. Immunol.

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Interleukin-22 (IL-22) is secreted by a wide range of immune cells and its downstream effects are mediated by the IL-22 receptor, which is present on non-immune cells in many organs throughout the body. IL-22 is an inflammatory mediator that conditions the tissue compartment by upregulating innate immune responses and is also a homeostatic factor that promotes tissue integrity and regeneration. Interestingly, the IL-22 system has also been linked to many T cell driven inflammatory diseases. Despite this, the downstream effects of IL-22 on the adaptive immune system has received little attention. We have reviewed the literature for experimental data that suggest IL-22 mediated effects on T cells, either transduced directly or via mediators expressed by innate immune cells or non-immune cells in response to IL-22. Collectively, the reviewed data indicate that IL-22 has a hitherto unappreciated influence on T helper cell polarization, or the secretion of signature cytokines, that is context dependent but in many cases results in a reduction of the Th1 type response and to some extent promotion of regulatory T cells. Further studies are needed that specifically address these aspects of IL-22 signaling, which can benefit the understanding and treatment of a wide range of diseases.

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IL-22 Binding Protein Promotes the Disease Process in Multiple Sclerosis

Cited by 17 publications

References 37 publications

Role of Th22 Cells in the Pathogenesis of Autoimmune Diseases

Role of Th22 Cells in the Pathogenesis of Autoimmune Diseases

IL-10 and IL-22 in Mucosal Immunity: Driving Protection and Pathology

Interleukin-22 Influences the Th1/Th17 Axis

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