Chronic inflammation is a critical response to potential danger signals caused by excessive and inappropriate inflammatory activity. Recently, a lot of pieces of evidence have proposed that the abnormal inflammatory response is closely associated with many chronic autoimmune diseases including systemic lupus erythematosus (SLE), inflammatory bowel disease (IBD), and type 1 diabetes. Patients suffering from autoimmune diseases have dramatically increased over the last decades. The increasing rates of these illnesses suggest that chronic inflammation could contribute to these diseases' pathology. Undoubtedly, these progressively debilitating conditions, and painful in some cases, can take a toll on people's quality of life and create societal and economic burdens. Scientists' ability to better understand the disease biology and pick out groups of patients through precision medicine, who will give a better response to specific treatments, can potentially lead to new and innovative medicines beyond broad immunosuppressive drugs.
Many studies have pointed out that the immune system plays a significant role in autoimmune diseases' pathogenesis by producing a variety of soluble mediators, including a group of secreted polypeptides known as cytokines. Cascade production of cytokines, down-regulation, negative feedback, and synergistic mechanisms are parameters that illustrate the connotation of "cytokine network" and worthily characterize the role of these mediators in the progression of severe inflammation to an autoimmune disorder. The interleukin-1 (IL-1) family of cytokines and receptors is unique in immunology due to their intimate relation with inflammation. They have long been recognized to play an essential role in the development of autoimmune diseases, including SLE and IBD. The IL-1 family is now comprised of 11 cytokines (IL-1a, IL-1ß, IL-18, IL-33, IL-36a, IL-36ß, IL-36?, IL-1R antagonist (IL-1Ra) while the IL-1 receptor family encompassed several members including IL-1R1, IL-1R2, IL-1R, IL-1RaP or IL- 1R3, IL-1R4, IL-18Ra, IL-36R, IL-18R, IL-18Rß or IL-1R7, IL-1R8, TIR8, IL-1R9, and IL-1R10. Information obtained in the last few years indicates that members of the IL-1 family are key players in the differentiation and function of innate immunity and adaptive immunity. Currently, a lot of missing data about many cytokines in the IL-1 family is present, and proved knowledge about newly discovered IL-1 family members (such as IL-37) and their role in autoimmune diseases is not fully elucidated. A better understanding of the pathophysiology of IL-1 and its relatives in autoimmunity involves a more in-depth evaluation of the possible abnormalities in the anti-inflammatory feedback mechanisms that might control inflammation holds the promise of innovative therapeutic tools and targets.
This Research Topic aims to shed some light on our current understanding of the IL-1 family members and their receptors and how they can be exploited as a noninvasive method for studying autoimmune disease progression and detecting biomarkers that may improve our personalized therapeutic strategies. We welcome the submission of Original Research articles, Reviews, and Mini-Reviews, which cover, but are not limited to, the following topics of interest:
1. Identification of cytokine signaling pathways in the IL-1 family and their participation in the progression of autoimmune diseases
2. Ability of cytokines belonged to the IL-1 family/their receptors to be used as a diagnosis, and prognosis biomarkers of autoimmune diseases
3. The new mechanism that might contribute to IL-1 family/receptor production regulating the development and progression of autoimmune diseases
4. Application of cytokine-based therapeutics in controlling autoimmune disease manifestations
Chronic inflammation is a critical response to potential danger signals caused by excessive and inappropriate inflammatory activity. Recently, a lot of pieces of evidence have proposed that the abnormal inflammatory response is closely associated with many chronic autoimmune diseases including systemic lupus erythematosus (SLE), inflammatory bowel disease (IBD), and type 1 diabetes. Patients suffering from autoimmune diseases have dramatically increased over the last decades. The increasing rates of these illnesses suggest that chronic inflammation could contribute to these diseases' pathology. Undoubtedly, these progressively debilitating conditions, and painful in some cases, can take a toll on people's quality of life and create societal and economic burdens. Scientists' ability to better understand the disease biology and pick out groups of patients through precision medicine, who will give a better response to specific treatments, can potentially lead to new and innovative medicines beyond broad immunosuppressive drugs.
Many studies have pointed out that the immune system plays a significant role in autoimmune diseases' pathogenesis by producing a variety of soluble mediators, including a group of secreted polypeptides known as cytokines. Cascade production of cytokines, down-regulation, negative feedback, and synergistic mechanisms are parameters that illustrate the connotation of "cytokine network" and worthily characterize the role of these mediators in the progression of severe inflammation to an autoimmune disorder. The interleukin-1 (IL-1) family of cytokines and receptors is unique in immunology due to their intimate relation with inflammation. They have long been recognized to play an essential role in the development of autoimmune diseases, including SLE and IBD. The IL-1 family is now comprised of 11 cytokines (IL-1a, IL-1ß, IL-18, IL-33, IL-36a, IL-36ß, IL-36?, IL-1R antagonist (IL-1Ra) while the IL-1 receptor family encompassed several members including IL-1R1, IL-1R2, IL-1R, IL-1RaP or IL- 1R3, IL-1R4, IL-18Ra, IL-36R, IL-18R, IL-18Rß or IL-1R7, IL-1R8, TIR8, IL-1R9, and IL-1R10. Information obtained in the last few years indicates that members of the IL-1 family are key players in the differentiation and function of innate immunity and adaptive immunity. Currently, a lot of missing data about many cytokines in the IL-1 family is present, and proved knowledge about newly discovered IL-1 family members (such as IL-37) and their role in autoimmune diseases is not fully elucidated. A better understanding of the pathophysiology of IL-1 and its relatives in autoimmunity involves a more in-depth evaluation of the possible abnormalities in the anti-inflammatory feedback mechanisms that might control inflammation holds the promise of innovative therapeutic tools and targets.
This Research Topic aims to shed some light on our current understanding of the IL-1 family members and their receptors and how they can be exploited as a noninvasive method for studying autoimmune disease progression and detecting biomarkers that may improve our personalized therapeutic strategies. We welcome the submission of Original Research articles, Reviews, and Mini-Reviews, which cover, but are not limited to, the following topics of interest:
1. Identification of cytokine signaling pathways in the IL-1 family and their participation in the progression of autoimmune diseases
2. Ability of cytokines belonged to the IL-1 family/their receptors to be used as a diagnosis, and prognosis biomarkers of autoimmune diseases
3. The new mechanism that might contribute to IL-1 family/receptor production regulating the development and progression of autoimmune diseases
4. Application of cytokine-based therapeutics in controlling autoimmune disease manifestations
