Editorial: Importance of cytokines and receptor members from the IL-1 family in the context of chronic autoimmune inflammatory diseases

COPYRIGHT © 2022 Talaat, Tabll, Gamal-Eldeen and Russo. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author (s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. TYPE Editorial PUBLISHED 19 July 2022 DOI 10.3389/fimmu.2022.974261

This Research Topic cover the recent advances in the role of several IL-1 family members, with particular emphasis on newly discovered IL-36, IL-37, and IL-38, in several autoimmune inflammatory diseases of the skin, gut, and teeth. The authors also discussed the role of cytokine gene polymorphism in disease susceptibility and pathogenesis. With the spread of COVID-19 infection worldwide and the ultimate need for vaccination, the efficacy and safety of COVID-19 vaccination in autoinflammatory rheumatic diseases under immunosuppressive drugs was discussed.
Periodontitis is a chronic inflammatory illness that causes tooth loss by destroying the tooth-supporting tissues (9), and cytokines are involved in periodontitis (10). Liu and Li looked at 147 publications with polymorphisms in 12 interleukins [Th1 (IL-2, IFN-g, and TNF-a), Th2 (IL-4 and IL-13), Th17 (IL-1a, IL-1b, IL-6, and IL-17), and Treg cytokines (IL-10 and TGF-b). Polymorphisms in the Th2 cytokine family, such as IL-4 and IL-13, have not been linked to periodontitis pathogenesis. However, Th17 cytokine genetic polymorphism may be a risk factor for periodontitis, while Treg cells may have a protective role in preventing periodontal inflammation. In this sense, IL-1 is an important cytokine biomarker in the development and progression of periodontitis.
Chronic inflammatory diseases may emerge in various tissues, including the skin, due to an imbalance in pro-and antiinflammatory cytokines from the IL-1 family As a member of the IL-1 cytokine family, IL-36 cytokines include the anti-inflammatory cytokine IL-36Ra and the proinflammatory cytokines IL-36a, IL-36b, and IL-36g (23). The most of the research has focused on its involvement in autoimmune diseases (24), but have demonstrated in the lung inflammation during infectious and non-infectious disorders (25)(26)(27). Peñaloza et al. review the current literature concerning the biology of IL-36 cytokines, including their synthesis and activation, also their impact on myeloid and lymphoid cells during inflammation. They also discussed their function during bacterial and viral lung infections, and other inflammatory lung disorders such as cancer, cystic fibrosis, allergic asthma, chronic obstructive pulmonary disease, and lung fibrosis. Peñaloza et al. also outline recent therapeutic development targeting the IL-36 pathway and the potential to treat lung inflammatory disorders.
The gastrointestinal tract (GIT) is lined by a single cell layer of intestinal epithelial cells (IECs) which are interconnected by the tight junctions (TJs), which serve as a gate or barrier to paracellular permeation of luminal contents (28). Disruption of the intestinal TJ barrier plays an essential role in the pathogenesis of several inflammatory conditions of the gut, including celiac disease and inflammatory bowel disease (IBD), characterized by elevated levels of IL-1 (28)(29)(30). In this review, Kaminsky et al. review most of the published studies that deal with the clinical consequences of IL-1b intestinal barrier regulation in intestinal inflammation, the underlying mechanisms and intracellular signaling pathways involved in TJ barrier permeability modulation, and the downstream molecular targets of IL-1b. Kaminsky et al. also discussed the potential therapeutic targeting of the TJ barrier.
In conclusion, this Research Topic highlights recent findings and new insights into the most recent development of the IL-1 family in the pathophysiology of several autoimmune diseases. The current research may provide new insight and advancements for future research targeting IL-1 in autoimmune diseases affecting teeth, skin, and GIT. Finally, in this Research Topic, the authors also go through elements of clinical translation and the biology of cytokines belonging to the IL-1 family in animal models, identifying potential targets for developing novel therapeutic approaches for autoimmunity.

Author contributions
RT, AT, AG-E and RR performed literature research, discussed the articles, and wrote the manuscript. All authors contributed to the article revision and approved the submitted version.

Funding
This work did not receive financial support for its design and publication. RR is fellow from National Council for Scientific and Technological Development (CNPq) [Grant number: 312839/2020-0], and the laboratory is supported by grant from