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Cellular and Molecular Biology in Autoimmune Disease
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Cellular and Molecular Biology in Autoimmune Disease

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

Deadline for manuscript submissions: closed (31 August 2022) | Viewed by 23839

Special Issue Editors

Prof. Dr. Cristina Belizna

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Guest Editor
Vascular and Coagulation Department, University Hospital Angers, 49100 Angers, France
Interests: antiphospholipid syndrome; OMICS; immune; autoimmune; rheumatology
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Pier Luigi Meroni

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Guest Editor
Immunorheumatology Research Laboratory, IRCCS Istituto Auxologico Italiano, 20145 Milano, Italy
Interests: autoimmunity; autoimmune disease; cellular biology; molecular biology; cellular pathways; self-tolerance; molecular mechanisms; pathogenesis; therapy
Special Issues, Collections and Topics in MDPI journals
Prof. Jaume Alijotas-Reig

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Guest Editor
1. Systemic Autoimmune Disease Unit, Department of Internal Medicine, Vall d’Hebron University Hospital, Barcelona, Spain
2. Department of Medicine, Universitat Autonòma, Barcelona, Spain
Interests: autoimmunity; autoimmune disease; cellular biology; molecular biology; cellular pathways; self-tolerance; molecular mechanisms; pathogenesis; therapy
Prof. Omar Latino

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Guest Editor
1. Autoimmune and Thrombophilic Disorders Department, Hospital Carlos G. Durand, Buenos Aires, Argentina
2. Hospital Carlos G. Durand, Buenos Aires, Argentina
Interests: autoimmunity; autoimmune disease; cellular biology; molecular biology; cellular pathways; self-tolerance; molecular mechanisms; pathogenesis; therapy

Special Issue Information

Dear Colleagues,

We are pleased to kindly invite you to contribute with your research to the special Issue: Cellular and Molecular Biology in Autoimmune Disease.

As autoimmune disease remain a major medical concern and the mechanisms responsible for their pathogenesis are still incompletely understood, new insights in this field are needed. Various cellular, molecular, and physiological mechanisms have been suggested as potential triggers for the loss of self-tolerance, which make immune cells unable to distinguish among “self” and “non-self” antigens. Cellular mechanisms coupled with various mechanisms at the molecular level initiate dysregulated intercellular communication and are involved in the pathogenesis of autoimmune disease. Both innate and acquired immune system have been determined to be involved at the molecular level.

New data into genetic susceptibility suggest that environmental triggers could act via cellular pathways containing disease-associated polymorphisms. The full and deep understanding of these mechanisms will allow an adapted therapy. Recent treatments are expected to simultaneously and specifically target several pathways in autoimmunity. Due to the heterogeneity of autoimmune mechanisms, the knowledge in this area are expected to lead to a personalized molecular medicine approach in the field of autoimmune disease. Your data are expected to contribute to new insights in this unravelled field and you are very welcome to join us.

Prof. Dr. Cristina Belizna
Prof. Dr. Pier Luigi Meroni
Prof. Jaume Alijotas-Reig
Prof. Omar Latino
Guest Editors

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
  • cellular biology
  • molecular biology
  • cellular pathways
  • self-tolerance
  • molecular mechanisms
  • pathogenesis
  • therapy
  • personalized molecular medicine

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Published Papers (6 papers)

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Research

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15 pages, 1976 KiB  
Article
Increased L-Selectin on Monocytes Is Linked to the Autoantibody Profile in Systemic Sclerosis
by Neža Brezovec, Katja Perdan-Pirkmajer, Tadeja Kuret, Blaž Burja, Snežna Sodin-Šemrl, Saša Čučnik and Katja Lakota
Int. J. Mol. Sci. 2022, 23(4), 2233; https://doi.org/10.3390/ijms23042233 - 17 Feb 2022
Cited by 4 | Viewed by 4829
Abstract
Monocytes are known to be implicated in the pathogenesis of systemic sclerosis (SSc), as they exert prominent migratory, adhesive, and chemotactic properties. The aim of our study was to characterize the surface expression of adhesion/chemotactic molecules (CD62L, CD11b, CCR2, CCR5) on the SSc [...] Read more.
Monocytes are known to be implicated in the pathogenesis of systemic sclerosis (SSc), as they exert prominent migratory, adhesive, and chemotactic properties. The aim of our study was to characterize the surface expression of adhesion/chemotactic molecules (CD62L, CD11b, CCR2, CCR5) on the SSc monocytes and determine correlations with the clinical presentation of SSc. We included 38 SSc patients and 36 healthy age-and sex-matched controls. Isolated monocytes, as well as in vitro serum-treated monocytes, were analyzed by flow cytometry; additionally, soluble CD62L was measured in serum. We found increased soluble CD62L in the SSc serum samples and increased CD62L on the surface of the SSc monocytes in the in the same set of patients. Among samples with determined SSc-specific autoantibodies, the surface CD62L was the lowest in patients positive for anti-PM/Scl autoantibodies and the highest in patients with anti-topoisomerase I autoantibodies (ATA). The treatment of isolated healthy monocytes with ATA-positive SSc serum resulted in increased surface CD62L expression. Moreover, surface CCR5 was reduced on the monocytes from SSc patients with interstitial lung disease but also, along with CCR2, negatively correlated with the use of analgesics/anti-inflammatory drugs and immunosuppressants. In conclusion, increased CD62L on SSc monocytes, particularly in ATA-positive patients, provides new insights into the pathogenesis of SSc and suggests CD62L as a potential therapeutic target. Full article
(This article belongs to the Special Issue Cellular and Molecular Biology in Autoimmune Disease)
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10 pages, 1651 KiB  
Article
Expression of DDX11 and DNM1L at the 12p11 Locus Modulates Systemic Lupus Erythematosus Susceptibility
by Mohammad Saeed, Alejandro Ibáñez-Costa, Alejandra María Patiño-Trives, Laura Muñoz-Barrera, Eduardo Collantes Estévez, María Ángeles Aguirre and Chary López-Pedrera
Int. J. Mol. Sci. 2021, 22(14), 7624; https://doi.org/10.3390/ijms22147624 - 16 Jul 2021
Cited by 2 | Viewed by 3754
Abstract
Objectives: This study employed genetic and functional analyses using OASIS meta-analysis of multiple existing GWAS and gene-expression datasets to identify novel SLE genes. Methods: Four hundred and ten genes were mapped using SNIPPER to 30 SLE GWAS loci and investigated for expression in [...] Read more.
Objectives: This study employed genetic and functional analyses using OASIS meta-analysis of multiple existing GWAS and gene-expression datasets to identify novel SLE genes. Methods: Four hundred and ten genes were mapped using SNIPPER to 30 SLE GWAS loci and investigated for expression in three SLE GEO-datasets and the Cordoba GSE50395-dataset. Blood eQTL for significant SNPs in SLE loci and STRING for functional pathways of differentially expressed genes were used. Confirmatory qPCR on SLE monocytes was performed. The entire 12p11 locus was investigated for genetic association using two additional GWAS. Expression of 150 genes at this locus was assessed. Based on this significance, qPCRs for DNM1L and KRAS were performed. Results: Fifty genes were differentially expressed in at least two SLE GEO-datasets, with all probes directionally aligned. DDX11, an RNA helicase involved in genome stability, was downregulated in both GEO and Cordoba datasets. The most significant SNP, rs3741869 in OASIS locus 12p11.21, containing DDX11, was a cis-eQTL regulating DDX11 expression. DDX11 was found repressed. The entire 12p11 locus showed three association peaks. Gene expression in GEO datasets identified DNM1L and KRAS, besides DDX11. Confirmatory qPCR validated DNM1L as an SLE susceptibility gene. DDX11, DNM1L and KRAS interact with each other and multiple known SLE genes including STAT1/STAT4 and major components of IFN-dependent gene expression, and are responsible for signal transduction of cytokines, hormones, and growth-factors, deregulation of which is involved in SLE-development. Conclusion: A genomic convergence approach with OASIS analysis of multiple GWAS and expression datasets identified DDX11 and DNM1L as novel SLE-genes, the expression of which is altered in monocytes from SLE patients. This study lays the foundation for understanding the pathogenic involvement of DDX11 and DNM1L in SLE by identifying them using a systems-biology approach, while the 12p11 locus harboring these genes was previously missed by four independent GWAS. Full article
(This article belongs to the Special Issue Cellular and Molecular Biology in Autoimmune Disease)
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20 pages, 4419 KiB  
Article
Disease Differentiation and Monitoring of Anti-TNF Treatment in Rheumatoid Arthritis and Spondyloarthropathies
by Katarzyna Bogunia-Kubik, Wojciech Wojtowicz, Jerzy Swierkot, Karolina Anna Mielko, Badr Qasem, Joanna Wielińska, Renata Sokolik, Łukasz Pruss and Piotr Młynarz
Int. J. Mol. Sci. 2021, 22(14), 7389; https://doi.org/10.3390/ijms22147389 - 9 Jul 2021
Cited by 4 | Viewed by 2988
Abstract
Rheumatoid arthritis (RA), ankylosing spondylitis (AS), and psoriatic arthritis (PsA) are comprehensive immunological disorders. The treatment of these disorders is limited to ameliorating the symptoms and improving the quality of life of patients. In this study, serum samples from RA, AS, and PsA [...] Read more.
Rheumatoid arthritis (RA), ankylosing spondylitis (AS), and psoriatic arthritis (PsA) are comprehensive immunological disorders. The treatment of these disorders is limited to ameliorating the symptoms and improving the quality of life of patients. In this study, serum samples from RA, AS, and PsA patients were analyzed with metabolomic tools employing the 1H NMR method in combination with univariate and multivariate analyses. The results obtained in this study showed that the changes in metabolites were the highest for AS > RA > PsA. The study demonstrated that the time until remission or until low disease activity is achieved is shortest (approximately three months) for AS, longer for RA and longest for PsA. The statistically common metabolite that was found to be negatively correlated with the healing processes of these disorders is ethanol, which may indicate the involvement of the gut microflora and/or the breakdown of malondialdehyde as a cell membrane lipid peroxide product. Full article
(This article belongs to the Special Issue Cellular and Molecular Biology in Autoimmune Disease)
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Review

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23 pages, 762 KiB  
Review
Practical Significance of Biomarkers in Axial Spondyloarthritis: Updates on Diagnosis, Disease Activity, and Prognosis
by Alexandra-Diana Diaconu, Alexandr Ceasovschih, Victorița Șorodoc, Cristina Pomîrleanu, Cătălina Lionte, Laurențiu Șorodoc and Codrina Ancuța
Int. J. Mol. Sci. 2022, 23(19), 11561; https://doi.org/10.3390/ijms231911561 - 30 Sep 2022
Cited by 13 | Viewed by 4205
Abstract
Axial spondyloarthritis (axSpA) is a chronic inflammatory disease that can lead to ankylosis by secondary ossification of inflammatory lesions, with progressive disability and a significant impact on quality of life. It is also a risk factor for the occurrence of comorbidities, especially cardiovascular [...] Read more.
Axial spondyloarthritis (axSpA) is a chronic inflammatory disease that can lead to ankylosis by secondary ossification of inflammatory lesions, with progressive disability and a significant impact on quality of life. It is also a risk factor for the occurrence of comorbidities, especially cardiovascular diseases (CVDs), mood disorders, osteoporosis, and malignancies. Early diagnosis and treatment are needed to prevent or decrease functional decline and to improve the patient’s prognosis. In respect of axSpA, there is an unmet need for biomarkers that can help to diagnose the disease, define disease activity and prognosis, and establish personalized treatment approaches. The aim of this review was to summarize the available information regarding the most promising biomarkers for axSpA. We classified and identified six core categories of biomarkers: (i) systemic markers of inflammation; (ii) molecules involved in bone homeostasis; (iii) HLA-B27 and newer genetic biomarkers; (iv) antibody-based biomarkers; (v) microbiome biomarkers; and (vi) miscellaneous biomarkers. Unfortunately, despite efforts to validate new biomarkers, few of them are used in clinical practice; however, we believe that these studies provide useful data that could aid in better disease management. Full article
(This article belongs to the Special Issue Cellular and Molecular Biology in Autoimmune Disease)
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18 pages, 1091 KiB  
Review
Inclusion Body Myositis and Neoplasia: A Narrative Review
by Laura Damian, Cristian Cezar Login, Carolina Solomon, Cristina Belizna, Svetlana Encica, Laura Urian, Ciprian Jurcut, Bogdan Stancu and Romana Vulturar
Int. J. Mol. Sci. 2022, 23(13), 7358; https://doi.org/10.3390/ijms23137358 - 1 Jul 2022
Cited by 9 | Viewed by 3717
Abstract
Inclusion body myositis (IBM) is an acquired, late-onset inflammatory myopathy, with both inflammatory and degenerative pathogenesis. Although idiopathic inflammatory myopathies may be associated with malignancies, IBM is generally not considered paraneoplastic. Many studies of malignancy in inflammatory myopathies did not include IBM patients. [...] Read more.
Inclusion body myositis (IBM) is an acquired, late-onset inflammatory myopathy, with both inflammatory and degenerative pathogenesis. Although idiopathic inflammatory myopathies may be associated with malignancies, IBM is generally not considered paraneoplastic. Many studies of malignancy in inflammatory myopathies did not include IBM patients. Indeed, IBM is often diagnosed only after around 5 years from onset, while paraneoplastic myositis is generally defined as the co-occurrence of malignancy and myopathy within 1 to 3 years of each other. Nevertheless, a significant association with large granular lymphocyte leukemia has been recently described in IBM, and there are reports of cancer-associated IBM. We review the pathogenic mechanisms supposed to be involved in IBM and outline the common mechanisms in IBM and malignancy, as well as the therapeutic perspectives. The terminally differentiated, CD8+ highly cytotoxic T cells expressing NK features are central in the pathogenesis of IBM and, paradoxically, play a role in some cancers as well. Interferon gamma plays a central role, mostly during the early stages of the disease. The secondary mitochondrial dysfunction, the autophagy and cell cycle dysregulation, and the crosstalk between metabolic and mitogenic pathways could be shared by IBM and cancer. There are intermingled subcellular mechanisms in IBM and neoplasia, and probably their co-existence is underestimated. The link between IBM and cancers deserves further interest, in order to search for efficient therapies in IBM and to improve muscle function, life quality, and survival in both diseases. Full article
(This article belongs to the Special Issue Cellular and Molecular Biology in Autoimmune Disease)
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17 pages, 718 KiB  
Review
Role of Distinct Macrophage Populations in the Development of Heart Failure in Macrophage Activation Syndrome
by Jakub Kuna, Zbigniew Żuber, Grzegorz Chmielewski, Leszek Gromadziński and Magdalena Krajewska-Włodarczyk
Int. J. Mol. Sci. 2022, 23(5), 2433; https://doi.org/10.3390/ijms23052433 - 23 Feb 2022
Cited by 6 | Viewed by 2788
Abstract
Macrophage activation syndrome (MAS) is one of the few entities in rheumatology with the potential to quickly cause multiple organ failure and loss of life, and as such, requires urgent clinical intervention. It has a broad symptomatology, depending on the organs it affects. [...] Read more.
Macrophage activation syndrome (MAS) is one of the few entities in rheumatology with the potential to quickly cause multiple organ failure and loss of life, and as such, requires urgent clinical intervention. It has a broad symptomatology, depending on the organs it affects. One especially dangerous aspect of MAS’s course of illness is myocarditis leading to acute heart failure and possibly death. Research in recent years has proved that macrophages settled in different organs are not a homogenous group, with particular populations differing in both structure and function. Within the heart, we can determine two major groups, based on the presence of the C-C 2 chemokine receptor (CCR2): CCR2+ and CCR2−. There are a number of studies describing their function and the changes in the population makeup between normal conditions and different illnesses; however, to our knowledge, there has not been one touching on the matter of changes occurring in the populations of heart macrophages during MAS and their possible consequences. This review summarizes the most recent knowledge on heart macrophages, the influence of select cytokines (those particularly significant in the development of MAS) on their activity, and both the immediate and long-term consequences of changes in the makeup of specific macrophage populations—especially the loss of CCR2− cells that are responsible for regenerative processes, as well as the substitution of tissue macrophages by the highly proinflammatory CCR2+ macrophages originating from circulating monocytes. Understanding the significance of these processes may lead to new discoveries that could improve the therapeutic methods in the treatment of MAS. Full article
(This article belongs to the Special Issue Cellular and Molecular Biology in Autoimmune Disease)
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