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Recent Advances in Autoimmune and Inflammatory Disorders
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Recent Advances in Autoimmune and Inflammatory Disorders

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: 20 May 2024 | Viewed by 12714

Special Issue Editor

Dr. Paola Galozzi

E-Mail Website
Guest Editor
Laboratory Medicine, Department of Medicine DIMED, University of Padova, Via Giustiniani, 2, 35128 Padova, Italy
Interests: autoimmunity; autoimmune disease; inflammatory disease; autoinflammatory diseases

Special Issue Information

Dear Colleagues,

I am pleased to invite you to contribute to this Special Issue of IJMS, entitled “Recent Advances in Autoimmune and Inflammatory Disorders”.

Inflammatory diseases encompass a wide range of disorders and conditions characterised by inflammation, from asthma to coeliac disease, and from autoimmune diseases to inflammatory bowel disease. Extensive research into the pathophysiology of these diseases has shown that various factors are involved in their pathogenesis. Since autoimmune and inflammatory diseases remain a major medical problem, the molecular mechanisms of which are still not fully understood, new knowledge is needed in this field.

Emerging data suggest that environmental triggers may act through peculiar cellular pathways. A comprehensive and deep understanding of these mechanisms will enable tailored therapy. Given the heterogeneity of autoimmune and inflammatory mechanisms, insights in this area are likely to lead to personalized molecular medicine. Cellular mechanisms coupled with various mechanisms at the molecular level have been proposed as a possible explanation for the loss of self-tolerance, whereby immune cells can no longer distinguish between "self" and "non-self" antigens.

Novel works ranging from basic and translational research at the molecular level, to pathogenetic mechanisms and clinical applications, are expected to contribute to new insights in this field. The submission of such works to this Special Issue is very welcome.

Dr. Paola Galozzi
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.

Keywords

  • autoimmunity
  • autoimmune disease
  • inflammation
  • inflammatory disease
  • cellular pathways
  • molecular mechanisms
  • pathogenesis
  • therapy

Published Papers (5 papers)

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Research

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14 pages, 1372 KiB  
Article
Serum Uric Acid Associates with Systemic Complement C3 Activation in Severe ANCA-Associated Renal Vasculitides
by Eva Baier, Ingmar Alexander Kluge, Samy Hakroush, Peter Korsten and Björn Tampe
Int. J. Mol. Sci. 2024, 25(2), 713; https://doi.org/10.3390/ijms25020713 - 05 Jan 2024
Viewed by 737
Abstract
Involvement of the complement system is key to the pathogenesis of antineutrophil cytoplasmic antibody (ANCA)-associated renal vasculitis, but immunometabolic implications, especially on serum uric acid (UA) levels, still need to be elucidated. A total of 34 patients with biopsy-proven ANCA-associated renal vasculitis between [...] Read more.
Involvement of the complement system is key to the pathogenesis of antineutrophil cytoplasmic antibody (ANCA)-associated renal vasculitis, but immunometabolic implications, especially on serum uric acid (UA) levels, still need to be elucidated. A total of 34 patients with biopsy-proven ANCA-associated renal vasculitis between 2015 and 2020 were retrospectively enrolled. Serum UA levels were correlated with clinical and histopathological characteristics, separated for critically ill (CI, n = 19), myeloperoxidase (MPO)-ANCA (n = 21) and proteinase 3 (PR3)-ANCA (n = 13) subgroups. We here identified inverse correlations of serum UA levels and complement C3 levels in the total cohort (p = 0.005) and the CI subgroup (p < 0.001). Intrarenal complement C4d deposition in venules correlated with serum UA levels in the total cohort (p = 0.007) and in the CI subgroup (p = 0.016). Significant associations of serum UA levels and tubulitis in areas of scarred cortex (t-IFTA) were identified in the total cohort (p = 0.008), and both subgroups of CI (p = 0.034) and MPO-ANCA (p = 0.029). In PR3-ANCA, interstitial fibrosis (ci) was observed as the strongest association with serum UA levels (p = 0.022). Our observations broaden our current understanding of contributory metabolic factors that influence the initial disease course in ANCA-associated renal vasculitis. Full article
(This article belongs to the Special Issue Recent Advances in Autoimmune and Inflammatory Disorders)
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Review

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18 pages, 1922 KiB  
Review
The NLRP3 Inflammasome as a Pathogenic Player Showing Therapeutic Potential in Rheumatoid Arthritis and Its Comorbidities: A Narrative Review
by Po-Ku Chen, Kuo-Tung Tang and Der-Yuan Chen
Int. J. Mol. Sci. 2024, 25(1), 626; https://doi.org/10.3390/ijms25010626 - 03 Jan 2024
Viewed by 1264
Abstract
Rheumatoid arthritis (RA) is an autoimmune inflammatory disease characterized by chronic synovitis and the progressive destruction of cartilage and bone. RA is commonly accompanied by extra-articular comorbidities. The pathogenesis of RA and its comorbidities is complex and not completely elucidated. The assembly of [...] Read more.
Rheumatoid arthritis (RA) is an autoimmune inflammatory disease characterized by chronic synovitis and the progressive destruction of cartilage and bone. RA is commonly accompanied by extra-articular comorbidities. The pathogenesis of RA and its comorbidities is complex and not completely elucidated. The assembly of the NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasome activates caspase-1, which induces the maturation of interleukin (IL)-1β and IL-18 and leads to the cleavage of gasdermin D with promoting pyroptosis. Accumulative evidence indicates the pathogenic role of NLRP3 inflammasome signaling in RA and its comorbidities, including atherosclerotic cardiovascular disease, osteoporosis, and interstitial lung diseases. Although the available therapeutic agents are effective for RA treatment, their high cost and increased infection rate are causes for concern. Recent evidence revealed the components of the NLRP3 inflammasome as potential therapeutic targets in RA and its comorbidities. In this review, we searched the MEDLINE database using the PubMed interface and reviewed English-language literature on the NLRP3 inflammasome in RA and its comorbidities from 2000 to 2023. The current evidence reveals that the NLRP3 inflammasome contributes to the pathogenesis of RA and its comorbidities. Consequently, the components of the NLRP3 inflammasome signaling pathway represent promising therapeutic targets, and ongoing research might lead to the development of new, effective treatments for RA and its comorbidities. Full article
(This article belongs to the Special Issue Recent Advances in Autoimmune and Inflammatory Disorders)
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17 pages, 1060 KiB  
Review
The Role of Short-Chain Fatty Acids and Altered Microbiota Composition in Autism Spectrum Disorder: A Comprehensive Literature Review
by Piotr P. Lagod and Saleh A. Naser
Int. J. Mol. Sci. 2023, 24(24), 17432; https://doi.org/10.3390/ijms242417432 - 13 Dec 2023
Cited by 1 | Viewed by 1250
Abstract
Autism spectrum disorder (ASD) is a complex neurodevelopmental condition characterized by deficits in communication and social interactions, restrictive and repetitive behavior, and a wide range of cognitive impediments. The prevalence of ASD tripled in the last 20 years and now affects 1 in [...] Read more.
Autism spectrum disorder (ASD) is a complex neurodevelopmental condition characterized by deficits in communication and social interactions, restrictive and repetitive behavior, and a wide range of cognitive impediments. The prevalence of ASD tripled in the last 20 years and now affects 1 in 44 children. Although ASD’s etiology is not yet elucidated, a growing body of evidence shows that it stems from a complex interplay of genetic and environmental factors. In recent years, there has been increased focus on the role of gut microbiota and their metabolites, as studies show that ASD patients show a significant shift in their gut composition, characterized by an increase in specific bacteria and elevated levels of short-chain fatty acids (SCFAs), especially propionic acid (PPA). This review aims to provide an overview of the role of microbiota and SCFAs in the human body, as well as possible implications of microbiota shift. Also, it highlights current studies aiming to compare the composition of the gut microbiome of ASD-afflicted patients with neurotypical control. Finally, it highlights studies with rodents where ASD-like symptoms or molecular hallmarks of ASD are evoked, via the grafting of microbes obtained from ASD subjects or direct exposure to PPA. Full article
(This article belongs to the Special Issue Recent Advances in Autoimmune and Inflammatory Disorders)
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17 pages, 589 KiB  
Review
Free Light Chains κ and λ as New Biomarkers of Selected Diseases
by Monika Gudowska-Sawczuk and Barbara Mroczko
Int. J. Mol. Sci. 2023, 24(11), 9531; https://doi.org/10.3390/ijms24119531 - 31 May 2023
Cited by 1 | Viewed by 5534
Abstract
Diagnostic and prognostic markers are necessary to help in patient diagnosis and the prediction of future clinical events or disease progression. As promising biomarkers of selected diseases, the free light chains (FLCs) κ and λ were considered. Measurements of FLCs are currently used [...] Read more.
Diagnostic and prognostic markers are necessary to help in patient diagnosis and the prediction of future clinical events or disease progression. As promising biomarkers of selected diseases, the free light chains (FLCs) κ and λ were considered. Measurements of FLCs are currently used in routine diagnostics of, for example, multiple myeloma, and the usefulness of FLCs as biomarkers of monoclonal gammopathies is well understood. Therefore, this review focuses on the studies concerning FLCs as new potential biomarkers of other disorders in which an inflammatory background has been observed. We performed a bibliometric review of studies indexed in MEDLINE to assess the clinical significance of FLCs. Altered levels of FLCs were observed both in diseases strongly connected with inflammation such as viral infections, tick-borne diseases or rheumatic disorders, and disorders that are moderately associated with immune system reactions, e.g., multiple sclerosis, diabetes, cardiovascular disorders and cancers. Increased concentrations of FLCs appear to be a useful prognostic marker in patients with multiple sclerosis or tick-borne encephalitis. Intensive synthesis of FLCs may also reflect the production of specific antibodies against pathogens such as SARS-CoV-2. Moreover, abnormal FLC concentrations might predict the development of diabetic kidney disease in patients with type 2 diabetes. Markedly elevated levels are also associated with increased risk of hospitalization and death in patients with cardiovascular disorders. Additionally, FLCs have been found to be increased in rheumatic diseases and have been related to disease activity. Furthermore, it has been suggested that inhibition of FLCs would reduce the progression of tumorigenesis in breast cancer or colitis-associated colon carcinogenesis. In conclusion, abnormal levels of κ and λ FLCs, as well as the ratio of κ:λ, are usually the result of disturbances in the synthesis of immunoglobulins as an effect of overactive inflammatory reactions. Therefore, it seems that κ and λ FLCs may be significant diagnostic and prognostic biomarkers of selected diseases. Moreover, the inhibition of FLCs appears to be a promising therapeutical target for the treatment of various disorders where inflammation plays an important role in the development or progression of the disease. Full article
(This article belongs to the Special Issue Recent Advances in Autoimmune and Inflammatory Disorders)
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23 pages, 1227 KiB  
Review
Autoimmunity: A New Focus on Nasal Polyps
by Jingyu Huang and Yu Xu
Int. J. Mol. Sci. 2023, 24(9), 8444; https://doi.org/10.3390/ijms24098444 - 08 May 2023
Cited by 3 | Viewed by 3183
Abstract
Chronic rhinosinusitis with nasal polyps (CRSwNP) has long been considered a benign, chronic inflammatory, and hyperplastic disease. Recent studies have shown that autoimmune-related mechanisms are involved in the pathology of nasal polyps. Activated plasma cells, eosinophils, basophils, innate type 2 lymphocytes, mast cells, [...] Read more.
Chronic rhinosinusitis with nasal polyps (CRSwNP) has long been considered a benign, chronic inflammatory, and hyperplastic disease. Recent studies have shown that autoimmune-related mechanisms are involved in the pathology of nasal polyps. Activated plasma cells, eosinophils, basophils, innate type 2 lymphocytes, mast cells, and proinflammatory cytokine in polyp tissue indicate the mobilization of innate and adaptive immune pathways during polyp formation. The discovery of a series of autoantibodies further supports the autoimmune nature of nasal polyps. Local homeostasis dysregulation, infection, and chronic inflammation may trigger autoimmunity through several mechanisms, including autoantigens overproduction, microbial translocation, molecular mimicry, superantigens, activation or inhibition of receptors, bystander activation, dysregulation of Toll-Like Receptors (TLRs), epitope spreading, autoantigens complementarity. In this paper, we elaborated on the microbiome-mediated mechanism, abnormal host immunity, and genetic changes to update the role of autoimmunity in the pathogenesis of chronic rhinosinusitis with nasal polyps. Full article
(This article belongs to the Special Issue Recent Advances in Autoimmune and Inflammatory Disorders)
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