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Updates in Cell and Molecular Mechanisms of Autoimmune Diseases

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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: closed (31 July 2023) | Viewed by 23769

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Prof. Dr. Kuender D. Yang

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Department of Medical Research, National Yang-Ming University Taiwan, Taipei, Taiwan
Interests: neonate; cytokines; T cells; epigenetics; L-arginine
Special Issues, Collections and Topics in MDPI journals

Prof. Dr. Lin-Shien Fu

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1. Department of Pediatrics, Taichung Veterans General Hospital, 1650 Taiwan Boulevard Sect. 4, Taichung 40705, Taiwan
2. Institute of Molecular Biology, National Chung Hsing University, Taichung 40227, Taiwan
3. Department of Pediatrics, National Yang-Ming University, Taipei 11221, Taiwan
Interests: complications of systemic lupus erythematosus; complements on vasculitis; target therapy of autoimmune disorders

Special Issue Information

Dear Colleagues,

The scope of the Special Issue of “Updates in Cell and Molecular Mechanisms of Autoimmune Disease” is to offer the possibility of collecting high-quality publications and to provide an interdisciplinary approach by submitting original papers, case series, and updated reviews on various aspects of autoimmune disorders including Kawasaki disease, type 1 diabetes, systemic lupus erythematosus, rheumatoid arthritis, vaccine-mediated autoimmunity including adjuvant effect, thyroid disease, thrombosis, and post-infectious (e.g. COVID-19) autoimmunity. The cell and molecular regulations of autoimmune diseases in central and peripheral immune systems are welcome to address the aspects of cell kinetics and/or molecular dynamics, particularly balance between Th17 and Treg development, for further precision target therapy. The identifications of epigenetic and/or genetic regulation of or predisposition to autoimmune diseases are also expected to provide for prediction and prevention. Physiological pathway interactions, theranostics of extracellular vesicles, alternative therapeutic strategies, and new methods in diseases or drug treatments for autoimmune disorders are also awaited.

Prof. Dr. Kuender D. Yang
Prof. Dr. Lin-Shien Fu
Guest Editors

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Keywords

adjuvant effect
autoimmune
cell kinetics
epigenetic
genetic regulation
interdisciplinary approach
kawasaki disease
molecular mechanisms
post-infectious (e.g. COVID-19) autoimmunity
rheumatoid arthritis
systemic lupus erythematosus
theranostics of extracellular vesicles
thrombosis
thyroid disease
type 1 diabetes
vaccine-mediated autoimmunity

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Published Papers (9 papers)

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Research

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16 pages, 4138 KiB

Open AccessArticle

The Influence of KE and EW Dipeptides in the Composition of the Thymalin Drug on Gene Expression and Protein Synthesis Involved in the Pathogenesis of COVID-19

by Natalia Linkova, Vladimir Khavinson, Anastasiia Diatlova, Michael Petukhov, Elizaveta Vladimirova, Maria Sukhareva and Anastasiia Ilina

Int. J. Mol. Sci. 2023, 24(17), 13377; https://doi.org/10.3390/ijms241713377 - 29 Aug 2023

Viewed by 1634

Abstract

Thymalin is an immunomodulatory drug containing a polypeptide extract of thymus that has demonstrated efficacy in the therapy of acute respiratory distress syndrome and chronic obstructive pulmonary disease, as well as in complex therapy related to severe COVID-19 in middle-aged and elderly patients.. KE and EW dipeptides are active substances of Thymalin. There is evidence that KE stimulates cellular immunity and nonspecific resistance in organisms, exerting an activating effect on macrophages, blood lymphocytes, thymocytes, and neutrophils, while EW reduces angiotensin-induced vasoconstriction and preserves endothelium-dependent vascular relaxation by inhibiting ACE2, the target protein of SARS-CoV-2. However, the mechanism of the immunomodulatory action of Thymalin, KE, and EW during COVID-19 remains unclear. To identify the potential mechanism of action underlying the immunomodulatory activity of Thymalin and its active components, EW and KE dipeptides, we assessed inflammatory response in the context of COVID-19. Interactions between EW and KE dipeptides and double-stranded DNA (dsDNA) were investigated by molecular modeling and docking using ICM-Pro. Analysis of the possible effect of EW and KE dipeptides on gene expression and protein synthesis involved in the pathogenesis of COVID-19 was conducted through the use of bioinformatics methods, including a search for promoter sequences in the Eukaryotic Promoter Database, the determination of genes associated with the development of COVID-19 using the PathCards database of human biological pathways (pathway unification database), identification of the relationship between proteins through cluster analysis in the STRING database (‘Search Tool for Retrieval of Interacting Genes/Proteins’), and assessment of the functional enrichment of protein–protein interaction (PPI) using the terms of gene ontology (GO) and the Markov cluster algorithm (MCL). After that, in vitro studying of a lipopolysaccharide (LPS)-induced model of inflammation using human peripheral blood mononuclear cells was performed. ELISA was applied to assess the level of cytokines (IL-1β, IL-6, TNFα) in the supernatant of cells with or without the impact of EW and KE peptides. Blood samples were obtained from four donors; for each cytokine, ELISA was performed 2–4 times, with two parallel experimental or control samples for each experiment (experiments to assess the effects of peptides on LPS-stimulated cells were repeated four times, while additional experiments with unstimulated cells were performed two times). Using molecular docking, GGAG was found to be the best dsDNA sequence in the classical B-form for binding the EW dipeptide, while GCGC is the preferred dsDNA sequence in the curved nucleosomal form for the KE dipeptide. Cluster analysis revealed that potential target genes for the EW and KE peptides encode the AKT1 and AKT2 proteins involved in the development of the cytokine storm. The specific targets for the EW peptide are the ACE2 and CYSLTR1 genes, and specific target for the KE peptide is the CHUK gene. Protein products of the ACE2, CYSLTR1, and CHUK genes are functionally associated with IL-1β, IL-6, TNF-α, IL-4, and IL-10 cytokines. An in vitro model of an inflammatory reaction demonstrated that Thymalin and EW and KE dipeptides reduced the synthesis of IL-1β, IL-6, and TNF-α cytokines in human peripheral blood mononuclear cells by 1.4–6.0 times. The immunomodulatory effect of Thymalin under the inflammatory response conditions in COVID-19 is based on the potential ability of its active components, EW and KE dipeptides, to regulate protein synthesis involved in the development of the cytokine storm. Full article

(This article belongs to the Special Issue Updates in Cell and Molecular Mechanisms of Autoimmune Diseases)

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12 pages, 2532 KiB

Open AccessArticle

IL-7 Deficiency Exacerbates Atopic Dermatitis in NC/Nga Mice

by Hyun Jung Park, Sung Won Lee, Luc Van Kaer, Myeong Sup Lee and Seokmann Hong

Int. J. Mol. Sci. 2023, 24(12), 9956; https://doi.org/10.3390/ijms24129956 - 9 Jun 2023

Cited by 2 | Viewed by 2197

Abstract

Interleukin-7 (IL-7) plays a vital role in the homeostasis of CD4⁺ and CD8⁺ T cells. Although IL-7 has been implicated in T helper (Th)1- and Th17-mediated autoinflammatory diseases, its role in Th2-type allergic disorders, such as atopic dermatitis (AD), remains unclear. Thus, to elucidate the effects of IL-7 deficiency on AD development, we generated IL-7-deficient AD-prone mice by backcrossing IL-7 knockout (KO) B6 mice onto the NC/Nga (NC) mouse strain, a model for human AD. As expected, IL-7 KO NC mice displayed defective development of conventional CD4⁺ and CD8⁺ T cells compared with wild type (WT) NC mice. However, IL-7 KO NC mice presented with enhanced AD clinical scores, IgE hyperproduction, and increased epidermal thickness compared with WT NC mice. Moreover, IL-7 deficiency decreased Th1, Th17, and IFN-γ-producing CD8⁺ T cells but increased Th2 cells in the spleen of NC mice, indicating that a reduced Th1/Th2 ratio correlates with severity of AD pathogenesis. Furthermore, significantly more basophils and mast cells infiltrated the skin lesions of IL-7 KO NC mice. Taken together, our findings suggest that IL-7 could be a useful therapeutic target for treating Th2-mediated skin inflammations, such as AD. Full article

(This article belongs to the Special Issue Updates in Cell and Molecular Mechanisms of Autoimmune Diseases)

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19 pages, 2477 KiB

Open AccessArticle

Association between Taxonomic Composition of Gut Microbiota and Host Single Nucleotide Polymorphisms in Crohn’s Disease Patients from Russia

by Maria Markelova, Anastasia Senina, Dilyara Khusnutdinova, Maria Siniagina, Elena Kupriyanova, Gulnaz Shakirova, Alfiya Odintsova, Rustam Abdulkhakov, Irina Kolesnikova, Olga Shagaleeva, Svetlana Lyamina, Sayar Abdulkhakov, Natalia Zakharzhevskaya and Tatiana Grigoryeva

Int. J. Mol. Sci. 2023, 24(9), 7998; https://doi.org/10.3390/ijms24097998 - 28 Apr 2023

Cited by 4 | Viewed by 1998

Abstract

Crohn’s disease (CD) is a chronic relapsing inflammatory bowel disease of unknown etiology. Genetic predisposition and dysbiotic gut microbiota are important factors in the pathogenesis of CD. In this study, we analyzed the taxonomic composition of the gut microbiota and genotypes of 24 single nucleotide polymorphisms (SNP) associated with the risk of CD. The studied cohorts included 96 CD patients and 24 healthy volunteers from Russia. Statistically significant differences were found in the allele frequencies for 8 SNPs and taxonomic composition of the gut microbiota in CD patients compared with controls. In addition, two types of gut microbiota communities were identified in CD patients. The main distinguishing driver of bacterial families for the first community type are Bacteroidaceae and unclassified members of the Clostridiales order, and the second type is characterized by increased abundance of Streptococcaceae and Enterobacteriaceae. Differences in the allele frequencies of the rs9858542 (BSN), rs3816769 (STAT3), and rs1793004 (NELL1) were also found between groups of CD patients with different types of microbiota communities. These findings confirm the complex multifactorial nature of CD. Full article

(This article belongs to the Special Issue Updates in Cell and Molecular Mechanisms of Autoimmune Diseases)

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11 pages, 1539 KiB

Open AccessArticle

The Role of New 3D Pathology and Lymphocyte Expression of Interstitial Inflammation in Pediatric-Onset Lupus Nephritis

by Yung-Chieh Huang, Yong-Chen Hsu, Jun-Pen Chen and Lin-Shien Fu

Int. J. Mol. Sci. 2023, 24(4), 3512; https://doi.org/10.3390/ijms24043512 - 9 Feb 2023

Viewed by 2454

Abstract

Lupus nephritis (LN) is a common and severe manifestation of pediatric-onset systemic lupus erythematosus (pSLE). It is one of the major causes of long-term glucocorticoid/immune suppressants use in pSLE. It causes long-term glucocorticoid/immune suppressants use and even end-stage renal disease (ESRD) in pSLE. It is now well known that high chronicity, especially the tubulointerstitial components in the renal biopsy, predicts a poor renal outcome. Interstitial inflammation (II), a component of activity in LN pathology, can be an early predictor for the renal outcome. With the advent of 3D pathology and CD19-targeted CAR-T cell therapy in the 2020s, the present study focuses on detailed pathology and B cell expression in II. We recruited 48 pSLE patients with class III/IV LN to analyze the risk of ESRD based on different II scores. We also studied 3D renal pathology and immunofluorescence (IF) staining of CD3, 19, 20, and 138 in patients with a high II score but low chronicity. Those pSLE LN patients with II scores of 2 or 3 showed a higher risk for ESRD (p = 0.003) than those with II scores of 0 or 1. Excluding patients with chronicity >3, high II scores still carried a higher risk for ESRD (p = 0.005). Checking the average scores from the renal specimens from different depths, the II, and chronicity showed good consistency between 3D and 2D pathology (interclass correlation coefficient [ICC], II = 0.91, p = 0.0015; chronicity = 0.86, p = 0.024). However, the sum of tubular atrophy plus interstitial fibrosis showed no good consistency (ICC = 0.79, p = 0.071). The selected LN patients with negative CD19/20 IF stains showed scattered CD3 infiltration and a different IF pattern of Syndecan-1 expression. Our study provides unique data in LN, including 3D pathology and different in situ Syndecan-1 patterns in LN patients. Full article

(This article belongs to the Special Issue Updates in Cell and Molecular Mechanisms of Autoimmune Diseases)

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18 pages, 1390 KiB

Open AccessArticle

Pathogenesis and Preventive Tactics of Immune-Mediated Non-Pulmonary COVID-19 in Children and Beyond

by Hsin Chi, Lung Chang, Yen-Chun Chao, Dar-Shong Lin, Horng-Woei Yang, Li-Ching Fang, Chia-Hsueh Lin, Che-Sheng Ho and Kuender D. Yang

Int. J. Mol. Sci. 2022, 23(22), 14157; https://doi.org/10.3390/ijms232214157 - 16 Nov 2022

Cited by 10 | Viewed by 2452

Abstract

The COVID-19 pandemic has evolved to immune escape and threatened small children and the elderly with a higher severity and fatality of non-pulmonary diseases. These life-threatening non-pulmonary COVID-19 diseases such as acute necrotizing encephalopathies (ANE) and multisystem inflammatory syndrome in children (MIS-C) are more prevalent in children. However, the mortality of multisystem inflammatory syndrome in adults (MIS-A) is much higher than that of MIS-C although the incidence of MIS-A is lower. Clarification of immunopathogenesis and genetic susceptibility of inflammatory non-pulmonary COVID-19 diseases would provide an appropriate guide for the crisis management and prevention of morbidity and fatality in the ongoing pandemic. This review article described three inflammatory non-pulmonary COVID-19 diseases including (1) meningoencephalitis (ME), (2) acute necrotizing encephalopathies (ANE), and (3) post-infectious multisystem inflammatory syndrome in children (MIS-C) and in adults (MIS-A). To prevent these life-threatening non-pulmonary COVID-19 diseases, hosts carrying susceptible genetic variants should receive prophylactic vaccines, avoid febrile respiratory tract infection, and institute immunomodulators and mitochondrial cocktails as early as possible. Full article

(This article belongs to the Special Issue Updates in Cell and Molecular Mechanisms of Autoimmune Diseases)

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31 pages, 9176 KiB

Open AccessArticle

Complementary Sets of Autoantibodies Induced by SARS-CoV-2, Adenovirus and Bacterial Antigens Cross-React with Human Blood Protein Antigens in COVID-19 Coagulopathies

by Robert Root-Bernstein, Jack Huber and Alison Ziehl

Int. J. Mol. Sci. 2022, 23(19), 11500; https://doi.org/10.3390/ijms231911500 - 29 Sep 2022

Cited by 8 | Viewed by 3377

Abstract

COVID-19 patients often develop coagulopathies including microclotting, thrombotic strokes or thrombocytopenia. Autoantibodies are present against blood-related proteins including cardiolipin (CL), serum albumin (SA), platelet factor 4 (PF4), beta 2 glycoprotein 1 (β2GPI), phosphodiesterases (PDE), and coagulation factors such as Factor II, IX, X and von Willebrand factor (vWF). Different combinations of autoantibodies associate with different coagulopathies. Previous research revealed similarities between proteins with blood clotting functions and SARS-CoV-2 proteins, adenovirus, and bacterial proteins associated with moderate-to-severe COVID-19 infections. This study investigated whether polyclonal antibodies (mainly goat and rabbit) against these viruses and bacteria recognize human blood-related proteins. Antibodies against SARS-CoV-2 and adenovirus recognized vWF, PDE and PF4 and SARS-CoV-2 antibodies also recognized additional antigens. Most bacterial antibodies tested (group A streptococci [GAS], staphylococci, Escherichia coli [E. coli], Klebsiella pneumoniae, Clostridia, and Mycobacterium tuberculosis) cross-reacted with CL and PF4. while GAS antibodies also bound to F2, Factor VIII, Factor IX, and vWF, and E. coli antibodies to PDE. All cross-reactive interactions involved antibody-antigen binding constants smaller than 100 nM. Since most COVID-19 coagulopathy patients display autoantibodies against vWF, PDE and PF4 along with CL, combinations of viral and bacterial infections appear to be necessary to initiate their autoimmune coagulopathies. Full article

(This article belongs to the Special Issue Updates in Cell and Molecular Mechanisms of Autoimmune Diseases)

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14 pages, 2167 KiB

Open AccessArticle

Expression of Eosinophilic Subtype Markers in Patients with Kawasaki Disease

by Ling-Sai Chang, Kuang-Den Chen, Ying-Hsien Huang and Ho-Chang Kuo

Int. J. Mol. Sci. 2022, 23(17), 10093; https://doi.org/10.3390/ijms231710093 - 3 Sep 2022

Cited by 2 | Viewed by 2222

Abstract

Purpose: Eosinophils may rise to a higher level in the acute phase of Kawasaki disease (KD) both before and after intravenous immunoglobulin (IVIG) therapy. A substantial body of research was carried out on the association between KD and allergic diseases. Eosinophils play an important role in type 2 inflammation. Recent studies have shown that there are two distinct subtypes of eosinophils. In addition to their role in inflammation, lung-resident eosinophils (rEOS) also regulate homeostasis. Inflammatory eosinophils (iEOS) reflect type 2 inflammation in tissues. iEOS were considered the primary eosinophils in non-severe allergic asthma, while rEOS were thought to be the primary eosinophils in severe non-allergic eosinophilic asthma. This case–control study aimed to investigate the marker expression of eosinophilic subtypes in KD patients. Materials and Methods: The marker expressions of eosinophilic subtypes in the leukocytes of patients with KD were evaluated by the recently established KDmarkers online tool, a web server including gene expression data. Finally, the results were validated with a quantitative reverse transcriptase polymerase chain reaction (RT-PCR). We analyzed the mRNA expression levels of SELL and IL10RA in leukocytes from KD patients and febrile children. Results: Included in our screening tools were transcriptome arrays, which provided clues showing the importance of rEOS, whose role was identified by three genes (lower IL10RA, higher SELL, and SERPINB1 than controls). In contrast, the iEOS representative gene CD101 was not elevated in KD. It was found that the gene IL10RA, a marker of inflammatory eosinophilic leukocytes, was more highly expressed in the leukocytes of KD patients (n = 43) than febrile controls (n = 32), especially those without coronary artery lesions (CAL) (n = 26). Before treatment, SELL expression was higher in leukocytes of CAL patients (CAL, 1.33 ± 0.18, n = 39; non-CAL, 0.87 ± 0.12, n = 55; p = 0.012). SELL was significantly higher after half a year compared to febrile controls. Conclusions: To our knowledge, this is the first study to demonstrate that KD patients have increased SELL than febrile controls after 6 months of treatment. We present evidence here that dynamically different eosinophilic involvement exists between KD patients with and without CAL. The role of eosinophilic subtypes in KD patients warrants further investigation. Full article

(This article belongs to the Special Issue Updates in Cell and Molecular Mechanisms of Autoimmune Diseases)

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Review

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11 pages, 429 KiB

Open AccessReview

Pathogenesis, Clinical Features, and Treatment of Patients with Myelin Oligodendrocyte Glycoprotein (MOG) Autoantibody-Associated Disorders Focusing on Optic Neuritis with Consideration of Autoantibody-Binding Sites: A Review

by Keiko Tanaka, Takeshi Kezuka, Hitoshi Ishikawa, Masami Tanaka, Kenji Sakimura, Manabu Abe and Meiko Kawamura

Int. J. Mol. Sci. 2023, 24(17), 13368; https://doi.org/10.3390/ijms241713368 - 29 Aug 2023

Cited by 5 | Viewed by 2622

Abstract

Although there is a substantial amount of data on the clinical characteristics, diagnostic criteria, and pathogenesis of myelin oligodendrocyte glycoprotein (MOG) autoantibody-associated disease (MOGAD), there is still uncertainty regarding the MOG protein function and the pathogenicity of anti-MOG autoantibodies in this disease. It is important to note that the disease characteristics, immunopathology, and treatment response of MOGAD patients differ from those of anti-aquaporin 4 antibody-positive neuromyelitis optica spectrum disorders (NMOSDs) and multiple sclerosis (MS). The clinical phenotypes of MOGAD are varied and can include acute disseminated encephalomyelitis, transverse myelitis, cerebral cortical encephalitis, brainstem or cerebellar symptoms, and optic neuritis. The frequency of optic neuritis suggests that the optic nerve is the most vulnerable lesion in MOGAD. During the acute stage, the optic nerve shows significant swelling with severe visual symptoms, and an MRI of the optic nerve and brain lesion tends to show an edematous appearance. These features can be alleviated with early extensive immune therapy, which may suggest that the initial attack of anti-MOG autoantibodies could target the structures on the blood–brain barrier or vessel membrane before reaching MOG protein on myelin or oligodendrocytes. To understand the pathogenesis of MOGAD, proper animal models are crucial. However, anti-MOG autoantibodies isolated from patients with MOGAD do not recognize mouse MOG efficiently. Several studies have identified two MOG epitopes that exhibit strong affinity with human anti-MOG autoantibodies, particularly those isolated from patients with the optic neuritis phenotype. Nonetheless, the relations between epitopes on MOG protein remain unclear and need to be identified in the future. Full article

(This article belongs to the Special Issue Updates in Cell and Molecular Mechanisms of Autoimmune Diseases)

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16 pages, 4553 KiB

Open AccessReview

The Role of B Cell and T Cell Glycosylation in Systemic Lupus Erythematosus

by Ivan Ramos-Martínez, Edgar Ramos-Martínez, Marco Cerbón, Armando Pérez-Torres, Laura Pérez-Campos Mayoral, María Teresa Hernández-Huerta, Margarito Martínez-Cruz, Alma Dolores Pérez-Santiago, Marco Antonio Sánchez-Medina, Iván Antonio García-Montalvo, Edgar Zenteno, Carlos Alberto Matias-Cervantes, Víctor Ojeda-Meixueiro and Eduardo Pérez-Campos

Int. J. Mol. Sci. 2023, 24(1), 863; https://doi.org/10.3390/ijms24010863 - 3 Jan 2023

Cited by 7 | Viewed by 3927

Abstract

Glycosylation is a post-translational modification that affects the stability, structure, antigenicity and charge of proteins. In the immune system, glycosylation is involved in the regulation of ligand–receptor interactions, such as in B-cell and T-cell activating receptors. Alterations in glycosylation have been described in several autoimmune diseases, such as systemic lupus erythematosus (SLE), in which alterations have been found mainly in the glycosylation of B lymphocytes, T lymphocytes and immunoglobulins. In immunoglobulin G of lupus patients, a decrease in galactosylation, sialylation, and nucleotide fucose, as well as an increase in the N-acetylglucosamine bisector, are observed. These changes in glycoisolation affect the interactions of immunoglobulins with Fc receptors and are associated with pericarditis, proteinuria, nephritis, and the presence of antinuclear antibodies. In T cells, alterations have been described in the glycosylation of receptors involved in activation, such as the T cell receptor; these changes affect the affinity with their ligands and modulate the binding to endogenous lectins such as galectins. In T cells from lupus patients, a decrease in galectin 1 binding is observed, which could favor activation and reduce apoptosis. Furthermore, these alterations in glycosylation correlate with disease activity and clinical manifestations, and thus have potential use as biomarkers. In this review, we summarize findings on glycosylation alterations in SLE and how they relate to immune system defects and their clinical manifestations. Full article

(This article belongs to the Special Issue Updates in Cell and Molecular Mechanisms of Autoimmune Diseases)

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