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Unveiling the Molecular Regulations of Immunological and Allergic 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 (30 September 2022) | Viewed by 11842

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Special Issue Editor

Prof. Dr. Agnieszka Paradowska‑Gorycka

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Guest Editor

National Institute of Geriatrics, Rheumatology and Rehabilitation, Warsaw, Poland
Interests: immune regulation; genotyping; genetics; cytokines; signaling pathways; autoimmune disorders; T cell biology; autoimmunity; inflammation; microRNA
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Special Issue Information

Dear Colleagues,

Immunological and Allergic Diseases are a major public health problem with no fully understood parthenogenesis. They are complex and heterogeneous diseases, where onset and disease course are dependent on interactions between different genetic/epigenetic and environmental or lifestyle factors. Although the exact immune-pathological mechanism of these diseases is not fully understood, numerous investigations have demonstrated abnormalities in CD4+ T cells and B cells, with a particular emphasis on T- and B-regulatory cells. More recently, a role for inherited epigenetic changes has also been demonstrated. Epigenetic mechanisms may serve as a dynamic link between the environment, genotypes, and phenotypes. Accumulating evidence has demonstrated that aberrant epigenetic modification plays a pivotal role in triggering the dysregulation of T/B-cell activation, thus leading to the occurrence of Immunological and Allergic Diseases. The articles in this Special Issue will cover important aspects in the area of molecular dysfunction in Immunological and Allergic Diseases and will present novel ideas for the diagnosis and treatment of these diseases, including molecular and cellular studies, correlation between genetics/epigenetics and phenotype of the disease, discovery of new subset of T and B cells, and personalized medicine.

Prof. Dr. Agnieszka Paradowska‑Gorycka
Guest Editor

Manuscript Submission Information

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Keywords

inflammation
T cells
B cells
genetic
epigenetic
molecular aspects
cytokines
therapy
immunotolerance

Published Papers (6 papers)

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Research

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14 pages, 4736 KiB

Open AccessArticle

Genetic Ablation of Nrf2 Exacerbates Neuroinflammation in Ocular Autoimmunity

by Yasuhiko Sato, Shoko Saito, Makiko Nakayama, Sunao Sugita, Akihiko Kudo and Hiroshi Keino

Int. J. Mol. Sci. 2022, 23(19), 11715; https://doi.org/10.3390/ijms231911715 - 3 Oct 2022

Cited by 4 | Viewed by 1769

Abstract

Experimental autoimmune uveoretinitis (EAU) is an animal model of non-infectious uveitis and is developed by immunization with retinal antigen, interphotoreceptor retinoid-binding protein (IRBP). Nuclear factor erythroid 2- (NF-E2-) related factor 2 (Nrf2) is responsible for regulating antioxidant and inflammatory responses. In this study, we investigated the role of Nrf2 on the development of EAU. Clinical and pathological examination demonstrated that retinal inflammation was exacerbated in Nrf2 knockout (Nrf2 KO) mice compared to wild type (WT) mice, and the expression of inflammatory cytokines (IFN-γ, IL-6, and IL-17) in the retina was significantly elevated in Nrf2 KO mice. GFAP positive cells (astrocytes) and Iba-1 positive cells (microglia cells) in the retina were more numerous in Nrf2 KO mice compared to WT mice. Furthermore, we examined the suppressive effect of the Nrf2 activator CDDO-Im (2-cyano-3,12 dioxooleana-1,9 dien-28-oyl imidazoline) on the development of EAU. The treatment with CDDO-Im significantly reduced the clinical and pathological score of EAU compared to those of vehicle-treated mice. These findings suggest that Nrf2 plays a regulatory role in the pathogenesis of autoimmune uveoretinitis and the activation of the Nrf2 system may have therapeutic potential for protecting vision from autoimmune neuroinflammation. Full article

(This article belongs to the Special Issue Unveiling the Molecular Regulations of Immunological and Allergic Diseases)

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11 pages, 1639 KiB

Open AccessArticle

Comparative Analysis of Serum microRNA in Diagnosed Ocular Sarcoidosis versus Idiopathic Uveitis with Ocular Manifestations of Sarcoidosis

by Shoko Saito, Hiroshi Keino, Ichiro Takasaki, Shinya Abe, Hideo Kohno, Kousuke Ichihara, Isami Hayashi, Makiko Nakayama, Yukihiro Tsuboshita, Sawako Miyoshi, Susumu Okamoto and Annabelle A. Okada

Int. J. Mol. Sci. 2022, 23(18), 10749; https://doi.org/10.3390/ijms231810749 - 15 Sep 2022

Cited by 2 | Viewed by 1548

Abstract

“Idiopathic” is the most common category of uveitis, representing cases in which a specific diagnosis has not been established despite work-up. Sarcoidosis is a systemic granulomatous disorder affecting multiple organs including the lungs, skin, kidneys, and eyes. We used microRNA (miRNA) microarrays to investigate serum miRNA profiles of patients with ocular sarcoidosis as diagnosed by specific criteria (diagnosed ocular sarcoidosis), and patients with idiopathic uveitis characterized by ocular manifestations of sarcoidosis (suspected ocular sarcoidosis). Principal component analysis (PCA) and hierarchical clustering showed that serum miRNA profiles of diagnosed ocular sarcoidosis and suspected ocular sarcoidosis were both clearly distinguishable from healthy controls. Furthermore, comparative analysis of the miRNA profiles showed highly similar patterns between diagnosed ocular sarcoidosis and suspected ocular sarcoidosis. Pathway analysis revealed common pathways were involved in the two groups, including those of WNT signaling and TGF-beta signaling. Our study demonstrated a high overlap of differentially expressed serum miRNAs in patients with diagnosed ocular sarcoidosis and suspected ocular sarcoidosis, suggesting that these groups share a similar underlying pathology and may represent possible variants of the disease. Characterization of serum miRNA profiles may provide an opportunity for earlier diagnosis and treatment, and may inform more accurate clinical prognosis in patients with an ocular sarcoidosis phenotype. Full article

(This article belongs to the Special Issue Unveiling the Molecular Regulations of Immunological and Allergic Diseases)

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14 pages, 1656 KiB

Open AccessArticle

Serum microRNAs in Systemic Sclerosis, Associations with Digital Vasculopathy and Lung Involvement

by Anna Wajda, Marcela Walczyk, Ewa Dudek, Barbara Stypińska, Aleksandra Lewandowska, Katarzyna Romanowska-Próchnicka, Marek Chojnowski, Marzena Olesińska and Agnieszka Paradowska-Gorycka

Int. J. Mol. Sci. 2022, 23(18), 10731; https://doi.org/10.3390/ijms231810731 - 14 Sep 2022

Cited by 7 | Viewed by 1627

Abstract

Background and aims: Systemic sclerosis (SSc) is an autoimmune, rare multisystem chronic disease that is still not well-understood aetiologically and is challenging diagnostically. In the literature, there are ever-increasing assumptions regarding the epigenetic mechanisms involved in SSc development; one of them is circulating microRNAs. Many of them regulate TLR pathways and are significant in autoimmune balance. The aim of this study was to determine profile expression of selected microRNAs in SSc patients, including miR-126, -132, -143, -145, -155, -181a, -29a and -3148, in comparison to healthy controls. Methods: Serum microRNAs were isolated from 45 patients with SSc and 57 healthy donors (HC). Additionally, SSc patients were considered in the aspect of disease subtype, including diffuse systemic sclerosis (dcSSc) and limited systemic sclerosis (lcSSc). Results: miR-3148 was detected neither in the serum of HC nor in SSc patients. All of the rest of the analyzed microRNAs, excluding miR-126, miR-29a and miR-181a, were significantly upregulated in SSc patients in comparison to HC. However, miR-181a has been revealed only in the serum of patients with lcSSc but not dcSSc. Moderate positive correlations between the transfer factor of the lung for carbon monoxide (TLCO) and miR-126 and miR-145 were observed. A significant correlation has been found between serum miR-143 level and forced vital capacity (FVC). SSc patients with FVC ≤ 70% were characterized by significantly lower levels of miR-143 compared to patients with normal FVC. Additionally, the expression of miR-132 was significantly higher in dcSSc subgroup with detected active lung lesions compared to dcSSc patients with fibrotic lesions. Patients with an early scleroderma pattern of microangiopathy seen on nailfold video-capillaroscopy (NVC) revealed higher expression of miR-155 in serum than those with a late pattern. Conclusions: The expression profile of circulating cell-free miRNAs is significantly changed in the serum of SSc patients compared to healthy individuals. Downregulation of miRNA-181a and overexpression of miR-132, miR-143, miR-145 and miR-155 in serum may be significant in SSc in the context of biomarkers. Full article

(This article belongs to the Special Issue Unveiling the Molecular Regulations of Immunological and Allergic Diseases)

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13 pages, 1904 KiB

Open AccessArticle

Molecular Allergen-Specific IgE Recognition Profiles and Cumulative Specific IgE Levels Associated with Phenotypes of Cat Allergy

by Ksenja Riabova, Antonina V. Karsonova, Marianne van Hage, Ulrika Käck, Jon R. Konradsen, Hans Grönlund, Daria Fomina, Evgeny Beltyukov, Polina A. Glazkova, Dmitry Yu. Semenov, Rudolf Valenta, Alexander Karaulov and Mirela Curin

Int. J. Mol. Sci. 2022, 23(13), 6984; https://doi.org/10.3390/ijms23136984 - 23 Jun 2022

Cited by 5 | Viewed by 2090

Abstract

Cat allergy is a major trigger factor for respiratory reactions (asthma and rhinitis) in patients with immunoglobulin E (IgE) sensitization. In this study, we used a comprehensive panel of purified cat allergen molecules (rFel d 1, nFel d 2, rFel d 3, rFel d 4, rFel d 7, and rFel d 8) that were obtained by recombinant expression in Escherichia coli or by purification as natural proteins to study possible associations with different phenotypes of cat allergy (i.e., rhinitis, conjunctivitis, asthma, and dermatitis) by analyzing molecular IgE recognition profiles in a representative cohort of clinically well-characterized adult cat allergic subjects (n = 84). IgE levels specific to each of the allergen molecules and to natural cat allergen extract were quantified by ImmunoCAP measurements. Cumulative IgE levels specific to the cat allergen molecules correlated significantly with IgE levels specific to the cat allergen extract, indicating that the panel of allergen molecules resembled IgE epitopes of the natural allergen source. rFel d 1 represented the major cat allergen, which was recognized by 97.2% of cat allergic patients; however, rFel d 3, rFel d 4, and rFel d 7 each showed IgE reactivity in more than 50% of cat allergic patients, indicating the importance of additional allergens in cat allergy. Patients with cat-related skin symptoms showed a trend toward higher IgE levels and/or frequencies of sensitization to each of the tested allergen molecules compared with patients suffering only from rhinitis or asthma, while there were no such differences between patients with rhinitis and asthma. The IgE levels specific to allergen molecules, the IgE levels specific to cat allergen extract, and the IgE levels specific to rFel d 1 were significantly higher in patients with four different symptoms compared with patients with 1–2 symptoms. This difference was more pronounced for the sum of IgE levels specific to the allergen molecules and to cat extract than for IgE levels specific for rFel d 1 alone. Our study indicates that, in addition to rFel d 1, rFel d 3, rFel d 4, and rFel d 7 must be considered as important cat allergens. Furthermore, the cumulative sum of IgE levels specific to cat allergen molecules seems to be a biomarker for identifying patients with complex phenotypes of cat allergy. These findings are important for the diagnosis of IgE sensitization to cats and for the design of allergen-specific immunotherapies for the treatment and prevention of cat allergy. Full article

(This article belongs to the Special Issue Unveiling the Molecular Regulations of Immunological and Allergic Diseases)

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Review

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26 pages, 2151 KiB

Open AccessReview

How an Immune-Factor-Based Formulation of Micro-Immunotherapy Could Interfere with the Physiological Processes Involved in the Atopic March

by Camille Jacques and Ilaria Floris

Int. J. Mol. Sci. 2023, 24(2), 1483; https://doi.org/10.3390/ijms24021483 - 12 Jan 2023

Cited by 5 | Viewed by 2338

Abstract

Allergic diseases consist of improper inflammatory reactions to antigens and are currently an important healthcare concern, especially considering their increasing worldwide development in recent decades. The “atopic march” defines the paradigm of allergic diseases occurring in chronological order and displaying specific spatial manifestations, as they usually start as atopic dermatitis (AD) and food allergies during infancy and progressively evolve into allergic asthma (AA) and allergic rhinitis (AR) or rhino-conjunctivitis in childhood. Many immune cell subtypes and inflammatory factors are involved in these hypersensitivity reactions. In particular, the T helpers 2 (Th2) subset, through its cytokine signatures made of interleukins (ILs), such as IL-4, IL-5, IL-10, and IL-13, as well as mast cells and their related histamine pathways, contribute greatly to the perpetuation and evolution of the atopic march. By providing low doses (LD) and ultra-low doses (ULD) of ILs and immune factors to the body, micro-immunotherapy (MI) constitutes an interesting therapeutic strategy for the management of the atopic march and its symptoms. One of the aims of this review is to shed light on the current concept of the atopic march and the underlying immune reactions occurring during the IgE-mediated responses. Moreover, the different classes of traditional and innovative treatments employed in allergic diseases will also be discussed, with a special emphasis on the potential benefits of the MI medicine 2LALERG^® formulation in this context. Full article

(This article belongs to the Special Issue Unveiling the Molecular Regulations of Immunological and Allergic Diseases)

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Other

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8 pages, 470 KiB

Open AccessCase Report

Autoimmune Neutropenia and Immune-Dysregulation in a Patient Carrying a TINF2 Variant

by Benedetta Chianucci, Alice Grossi, Gianluca Dell'Orso, Elena Palmisani, Marina Lanciotti, Paola Terranova, Filomena Pierri, Michela Lupia, Luca Arcuri, Marica Laurino, Isabella Ceccherini, Fabian Beier, Carlo Dufour, Francesca Fioredda and Maurizio Miano

Int. J. Mol. Sci. 2022, 23(23), 14535; https://doi.org/10.3390/ijms232314535 - 22 Nov 2022

Cited by 1 | Viewed by 1520

Abstract

In recent years, the knowledge about the immune-mediated impairment of bone marrow precursors in immune-dysregulation and autoimmune disorders has increased. In addition, immune-dysregulation, secondary to marrow failure, has been reported as being, in some cases, the most evident and early sign of the disease and making the diagnosis of both groups of disorders challenging. Dyskeratosis congenita is a disorder characterized by premature telomere erosion, typically showing marrow failure, nail dystrophy and leukoplakia, although incomplete genetic penetrance and phenotypes with immune-dysregulation features have been described. We report on a previously healthy 17-year-old girl, with a cousin successfully treated for acute lymphoblastic leukemia, who presented with leukopenia and neutropenia. The diagnostic work-up showed positive anti-neutrophil antibodies, leading to the diagnosis of autoimmune neutropenia, a slightly low NK count and high TCR-αβ+-double-negative T-cells. A next-generation sequencing (NGS) analysis showed the 734C>A variant on exon 6 of the TINF2 gene, leading to the p.Ser245Tyr. The telomere length was short on the lymphocytes and granulocytes, suggesting the diagnosis of an atypical telomeropathy showing with immune-dysregulation. This case underlines the importance of an accurate diagnostic work-up of patients with immune-dysregulation, who should undergo NGS or whole exome sequencing to identify specific disorders that deserve targeted follow-up and treatment. Full article

(This article belongs to the Special Issue Unveiling the Molecular Regulations of Immunological and Allergic Diseases)

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