BACKGROUND: There is an increasing number of patients following hernia surgery with implanted mesh reporting symptoms that could indicate autoimmune or allergic reactions to mesh. 'Allergy' to metals, various drugs, and chemicals is well recognised. However, hypersensitivity, allergy or autoimmunity caused by surgical mesh has not been proven by a scientific method to date. The aim of this study was twofold: to describe the pathophysiology of autoimmunity and foreign body reaction and to undertake a systematic review of surgical mesh implanted at the time of hernia repair and the subsequent development of autoimmune disease. METHODS: A systematic review using the PRISMA guidelines was undertaken. Pubmed (Medline), Google Scholar and Cochrane databases were searched for all English-written peer-reviewed articles published between 2000 and 2021. The search was performed using the keywords "hernia", "mesh", "autoimmunity", "ASIA", "immune response", "autoimmune response". RESULTS: Seven papers were included in the final analysis-three systematic reviews, three cohort studies and one case report. Much of the current data regarding the association of hernia mesh and autoimmunity relies on retrospective cohort studies and/or case reports with limited availability of cofounding factor data linked to autoimmune disease such as smoking status or indeed a detailed medical history of patients. Three systematic reviews have discussed this topic, each with a slightly different approach and none of them has identified causality between the use of mesh and the subsequent development of autoimmune disease. CONCLUSION: There is little evidence that the use of polypropylene mesh can lead to autoimmunity. A large number of potential triggers of autoimmunity along with the genetic predisposition to autoimmune disease and the commonality of hernia, make a cause and effect difficult to unravel at present. Biomaterials cause foreign body reactions, but a chronic foreign body reaction does not indicate autoimmunity, a common misunderstanding in the literature.

• Keywords
• ASIA, Autoimmune, Autoimmunity, Hernia mesh, Immune, Polypropylene,
• MeSH
• Autoimmune Diseases * etiology   MeSH
• Surgical Mesh adverse effects   MeSH
• Hernia, Inguinal * surgery   MeSH
• Humans MeSH
• Herniorrhaphy adverse effects   methods   MeSH
• Foreign-Body Reaction surgery   MeSH
• Retrospective Studies MeSH
• Check Tag
• Humans MeSH
• Publication type
• Journal Article MeSH
• Case Reports MeSH
• Research Support, Non-U.S. Gov't MeSH
• Systematic Review MeSH

Asthma and chronic rhinosinusitis with nasal polyps (CRSwNP) or without (CRSsNP) are chronic respiratory diseases. These two disorders often co-exist based on common anatomical, immunological, histopathological, and pathophysiological basis. Usually, asthma with comorbid CRSwNP is driven by type 2 (T2) inflammation which predisposes to more severe, often intractable, disease. In the past two decades, innovative technologies and detection techniques in combination with newly introduced targeted therapies helped shape our understanding of the immunological pathways underlying inflammatory airway diseases and to further identify several distinct clinical and inflammatory subsets to enhance the development of more effective personalized treatments. Presently, a number of targeted biologics has shown clinical efficacy in patients with refractory T2 airway inflammation, including anti-IgE (omalizumab), anti-IL-5 (mepolizumab, reslizumab)/anti-IL5R (benralizumab), anti-IL-4R-α (anti-IL-4/IL-13, dupilumab), and anti-TSLP (tezepelumab). In non-type-2 endotypes, no targeted biologics have consistently shown clinical efficacy so far. Presently, multiple therapeutical targets are being explored including cytokines, membrane molecules and intracellular signalling pathways to further expand current treatment options for severe asthma with and without comorbid CRSwNP. In this review, we discuss existing biologics, those under development and share some views on new horizons.

• Keywords
• airway remodelling, asthma, biologics, chronic rhinosinusitis, precision medicine, type 2 inflammation,
• MeSH
• Biological Products * therapeutic use   MeSH
• Asthma * complications   drug therapy   epidemiology   MeSH
• Chronic Disease MeSH
• Comorbidity MeSH
• Humans MeSH
• Nasal Polyps * complications   drug therapy   MeSH
• Rhinitis * complications   drug therapy   MeSH
• Sinusitis * complications   drug therapy   MeSH
• Inflammation drug therapy   MeSH
• Check Tag
• Humans MeSH
• Publication type
• Journal Article MeSH
• Review MeSH
• Names of Substances
• Biological Products * MeSH

Kidney allograft transplantation improved the prognosis and quality of life of patients with end-stage renal diseases but the occurrence of acute rejection represents a limitation of the final outcome. Noninvasive biomarkers are needed as well as further advancements in the understanding of immune mechanisms of reaction to the allograft. Our study of 138 patients focused on one-year monitoring of serum concentrations of 12 chemokines regulating the recruitment of different immune cells into transplanted allograft and on in vitro regulation of the same chemokines release by interactions of renal proximal epithelial cells with monocyte/macrophage cell line stimulated with TNF alpha. In a group of 44 patients with acute rejection, higher serum pretransplant levels of CXCL1, CXCL5, CXCL6, CCL2, CCL21, and particularly CXCL10 and CX3CL1(both p < 0.001) were found suggesting their higher proinflammatory status as compared to subjects with the uncomplicated outcome. In samples collected at the day of biopsy positive for acute rejection, chemokines CXCL9 and CXCL11 attracting preferentially Th1 lymphocytes were found to be upregulated. In our in vitro model with TNF alpha induction, renal proximal epithelial cells seemed to be a more potent source of chemokines attracting neutrophils as compared to monocyte/macrophage cell line but the coculture of these cells potentiated release of neutrophilic chemokines CXCL5 and CXCL6. Similar augmentation of chemokine production was found also in the case of CCL2. On the other hand, adding of monocytes/macrophages to a culture of renal epithelial cells suppressed the release of CXCL10 and CXCL11 attracting T lymphocytes. We assume from our data that in kidney allograft transplantation, chemokines attracting neutrophils, T lymphocytes, and monocytes are induced simultaneously and measurement some of them in combination might be used as biomarkers of acute rejection. Mutual cell-cell interactions of immune cells with renal parenchyma seem to be important for fine regulation of chemokine release.

• MeSH
• Allografts MeSH
• Chemokine CCL2 blood   MeSH
• Chemokine CCL21 blood   MeSH
• Chemokine CX3CL1 blood   MeSH
• Chemokine CXCL1 blood   MeSH
• Chemokine CXCL10 blood   MeSH
• Chemokine CXCL11 blood   MeSH
• Chemokine CXCL5 blood   MeSH
• Chemokine CXCL6 blood   MeSH
• Chemokine CXCL9 blood   MeSH
• Chemokines blood   MeSH
• Quality of Life MeSH
• Humans MeSH
• Graft Rejection blood   immunology   MeSH
• Th1 Cells metabolism   MeSH
• Kidney Transplantation adverse effects   MeSH
• Check Tag
• Humans MeSH
• Publication type
• Journal Article MeSH
• Names of Substances
• Chemokine CCL2 MeSH
• Chemokine CCL21 MeSH
• Chemokine CX3CL1 MeSH
• Chemokine CXCL1 MeSH
• Chemokine CXCL10 MeSH
• Chemokine CXCL11 MeSH
• Chemokine CXCL5 MeSH
• Chemokine CXCL6 MeSH
• Chemokine CXCL9 MeSH
• Chemokines MeSH
• CXCL1 protein, human MeSH Browser

Autoinflammatory diseases (AIDs) represent a rare and heterogeneous group of disorders characterized by recurrent episodes of inflammation and a broad range of clinical manifestations. The most common symptoms involve recurrent fevers, musculoskeletal symptoms, and serositis; however, AIDs can also lead to life-threatening complications, such as macrophage activation syndrome (MAS) and systemic AA amyloidosis. Typical monogenic periodic fever syndromes include cryopyrin-associated periodic fever syndrome (CAPS), tumor necrosis factor receptor-associated periodic syndrome (TRAPS), mevalonate kinase deficiency/hyper IgD syndrome (MKD/HIDS), and familial Mediterranean fever (FMF). However, a number of other clinical entities, such as systemic juvenile idiopathic arthritis (sJIA), adult-onset Still's disease (AOSD), Kawasaki disease (KD) and idiopathic recurrent pericarditis (IRP), display similar phenotypical and immunological features to AIDs. All these diseases are pathophysiologicaly characterized by dysregulation of the innate immune system and the central pathogenic role is attributed to the IL-1 cytokine family (IL-1α, IL-1β, IL-1Ra, IL-18, IL-36Ra, IL-36α, IL-37, IL-36β, IL-36g, IL-38, and IL-33). Therefore, reasonable therapeutic approaches aim to inhibit these cytokines and their pathways. To date, several anti-IL-1 therapies have evolved. Each drug differs in structure, mechanism of action, efficacy for the treatment of selected diseases, and side effects. Most of the available data regarding the efficacy and safety of IL-1 inhibitors are related to anakinra, canakinumab, and rilonacept. Other promising therapeutics, such as gevokizumab, tadekinig alfa, and tranilast are currently undergoing clinical trials. In this review, we provide sophisticated and up-to-date insight into the therapeutic uses of different IL-1 inhibitors in monogenic periodic fever syndromes.

• Keywords
• CAPS, FMF, IL-1, TRAPS, anakinra, canakinumab, rilonacept,
• MeSH
• Anti-Inflammatory Agents therapeutic use   MeSH
• Hereditary Autoinflammatory Diseases drug therapy   immunology   MeSH
• Interleukin-1 antagonists & inhibitors   MeSH
• Humans MeSH
• Check Tag
• Humans MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Review MeSH
• Names of Substances
• Anti-Inflammatory Agents MeSH
• Interleukin-1 MeSH