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IL-36 Family Cytokines in Physiological and Pathophysiological Inflammation
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IL-36 Family Cytokines in Physiological and Pathophysiological Inflammation

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: closed (31 December 2022) | Viewed by 3526

Special Issue Editor

Dr. Andreas Weigert

E-Mail Website
Guest Editor
Institute of Biochemistry I, Faculty of Medicine, Goethe-University Frankfurt, 60590 Frankfurt, Germany
Interests: macrophage biology; cytokines; resolution of inflammation; tumor immunology; lipid signaling; apoptosis; innate-like lymphocytes; multispectral imaging
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

The IL-36 family of cytokines is a poorly understood subfamily of the IL-1 family. It consists of three pro-inflammatory receptor agonists: IL-36α, IL-36β, IL-36γ; one IL-36 receptor (IL-1R6) antagonist: IL-36RA; and one putative IL-1R6 antagonist: IL-38. Experimental data suggest that IL-36 family cytokines play a role in the protection of barrier tissues from infection, but also in the auto-inflammatory disorders in these tissues. The most prominent example of this is most likely the increased susceptibility to generalized pustular psoriasis, which is caused by mutations in IL-36RA. There is still much to learn about the function of IL-36 family cytokines in inflammatory disorders, including auto-immunity and cancer. Therefore, this Special Issue welcomes original research and review articles that focus on the molecular aspects of IL-36 family signaling in physiological and pathophysiological inflammation.

Dr. Andreas Weigert
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Published Papers (2 papers)

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Research

11 pages, 1399 KiB  
Article
Opposing Effects of Interleukin-36γ and Interleukin-38 on Trained Immunity
by Lisa U. Teufel, Mihai G. Netea, Frank L. van de Veerdonk, Charles A. Dinarello, Leo A. B. Joosten and Rob J. W. Arts
Int. J. Mol. Sci. 2023, 24(3), 2311; https://doi.org/10.3390/ijms24032311 - 24 Jan 2023
Cited by 3 | Viewed by 1778
Abstract
Trained immunity is the process of long-term functional reprogramming (a de facto innate immune memory) of innate immune cells such as monocytes and macrophages after an exposure to pathogens, vaccines, or their ligands. The induction of trained immunity is mediated through epigenetic and [...] Read more.
Trained immunity is the process of long-term functional reprogramming (a de facto innate immune memory) of innate immune cells such as monocytes and macrophages after an exposure to pathogens, vaccines, or their ligands. The induction of trained immunity is mediated through epigenetic and metabolic mechanisms. Apart from exogenous stimuli, trained immunity can be induced by endogenous compounds such as oxidized LDL, urate, fumarate, but also cytokines including IL-1α and IL-1β. Here, we show that also recombinant IL-36γ, a pro-inflammatory cytokine of the IL-1-family, is able to induce trained immunity in primary human monocytes, demonstrated by higher cytokine responses and an increase in cellular metabolic pathways both regulated by epigenetic histone modifications. These effects could be inhibited by the IL-36 receptor antagonist as well as by IL-38, an anti-inflammatory cytokine of the IL-1 family which shares its main receptor with IL-36 (IL-1R6). Further, we demonstrated that trained immunity induced by IL-36γ is mediated by NF-κB and mTOR signaling. The inhibitory effect of IL-38 on IL-36γ-induced trained immunity was confirmed in experiments using bone marrow of IL-38KO and WT mice. These results indicate that exposure to IL-36γ results in long-term pro-inflammatory changes in monocytes which can be inhibited by IL-38. Recombinant IL-38 could therefore potentially be used as a therapeutic intervention for diseases characterized by exacerbated trained immunity. Full article
(This article belongs to the Special Issue IL-36 Family Cytokines in Physiological and Pathophysiological Inflammation)
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13 pages, 2818 KiB  
Article
MES SV40 Cells Are Sensitive to Lipopolysaccharide, Peptidoglycan, and Poly I:C Expressing IL-36 Cytokines
by Cesar G. Pelcastre-Rodriguez, Ernesto A. Vazquez-Sanchez, José M. Murrieta-Coxca, Sandra Rodríguez-Martínez, Juan C. Cancino-Diaz and Mario E. Cancino-Diaz
Int. J. Mol. Sci. 2022, 23(19), 11922; https://doi.org/10.3390/ijms231911922 - 07 Oct 2022
Viewed by 1340
Abstract
Mesangial cells (MC) maintain the architecture and cellular communication and indirectly join in the glomerular filtration rate for the correct functioning of the glomerulus. Consequently, these cells are activated constantly in response to changes in the intraglomerular environment due to a metabolic imbalance [...] Read more.
Mesangial cells (MC) maintain the architecture and cellular communication and indirectly join in the glomerular filtration rate for the correct functioning of the glomerulus. Consequently, these cells are activated constantly in response to changes in the intraglomerular environment due to a metabolic imbalance or infection. IL-36, a member of the IL-1 family, is a cytokine that initiates and maintains inflammation in different tissues in acute and chronic pathologies, including the skin, lungs, and intestines. In the kidney, IL-36 has been described in the development of tubulointerstitial lesions, the production of an inflammatory environment, and is associated with metabolic and mesangioproliferative disorders. The participation of IL-36 in functional dysregulation and the consequent generation of the inflammatory environment by MCs in the presence of microbial stimulation is not yet elucidated. In this work, the MES SV40 cell cultures were stimulated with classical pathogen-associated molecular patterns (PAMPs), mimicking an infection by negative and positive bacteria as well as a viral infection. Lipopolysaccharide (LPS), peptidoglycan (PGN) microbial wall components, and a viral mimic poly I:C were used, and the mRNA and protein expression of the IL-36 members were assessed. We observed a differential and dose-dependent IL-36 mRNA and protein expression under LPS, PGN, and poly I:C stimulation. IL-36β was only found when the cells were treated with LPS, while IL-36α and IL-36γ were favored by PGN and poly I:C stimulation. We suggest that the microbial components participate in the activation of MCs, leading them to the production of IL-36, in which a specific member may participate in the origin and maintenance of inflammation in the glomerular environment that is associated with infections. Full article
(This article belongs to the Special Issue IL-36 Family Cytokines in Physiological and Pathophysiological Inflammation)
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