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Molecular Aspects of Autoimmune Diseases
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Molecular Aspects of Autoimmune Diseases

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: 30 June 2024 | Viewed by 3649

Special Issue Editor

Dr. Raquel López Mejías

E-Mail Website
Guest Editor
Immunopathology Group on Systemic Inflammatory Diseases, IDIVAL, 39011 Santander, Spain
Interests: genetics; epigenetics; molecules; cellules; autoimmune diseases; mechanisms; inflammation

Special Issue Information

Dear Colleagues,

Autoimmune diseases are a group of pathologies characterized by an abnormal immune response, inflammatory symptoms and tissue damage. Clinical differences have been described among them, although they share common molecular mechanisms. Interestingly, these specific molecular mechanisms are still unknown. In this regard, identifying these molecular mechanisms (at genetic, epigenetic, molecular and cellular levels) is an issue of great importance in order to establish an early and accurate diagnosis of each autoimmune disease, preventing the development of the comorbidities associated with them. In addition, identifying the molecular mechanisms underlying autoimmune diseases allows us to develop therapeutic strategies more specific to the treatment of these conditions. In this Special Issue, we invite authors to submit original research and review articles contributing to a better understanding of the following topics which include, but are not limited to, the role of genetics in autoimmune diseases, the role of epigenetics in autoimmune diseases, the molecules and cellules implicated in autoimmune diseases and the molecular mechanisms implicated in the development of autoimmune disease comorbidities.

Dr. Raquel López Mejías
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

  • genetics
  • epigenetics
  • molecules
  • cellules
  • autoimmune diseases
  • inflammation

Published Papers (3 papers)

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Research

15 pages, 4374 KiB  
Article
Effect of the Functional VP1 Unique Region of Human Parvovirus B19 in Causing Skin Fibrosis of Systemic Sclerosis
by Der-Yuan Chen, Chih-Chen Tzang, Chuan-Ming Liu, Tsu-Man Chiu, Jhen-Wei Lin, Pei-Hua Chuang, Chia-Wei Kuo, Bor-Show Tzang and Tsai-Ching Hsu
Int. J. Mol. Sci. 2023, 24(20), 15294; https://doi.org/10.3390/ijms242015294 - 18 Oct 2023
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Abstract
Human parvovirus B19 (B19V) is a single-stranded non-enveloped DNA virus of the family Parvoviridae that has been associated with various autoimmune disorders. Systemic sclerosis (SSc) is an autoimmune connective tissue disorder with high mortality and has been linked to B19V infection. However, the [...] Read more.
Human parvovirus B19 (B19V) is a single-stranded non-enveloped DNA virus of the family Parvoviridae that has been associated with various autoimmune disorders. Systemic sclerosis (SSc) is an autoimmune connective tissue disorder with high mortality and has been linked to B19V infection. However, the precise mechanism underlying the B19V contribution to the development of SSc remains uncertain. This study investigated the impacts of the functional B19V-VP1 unique region (VP1u) in macrophages and bleomycin (BLE)-induced SSc mice. Cell experimental data showed that significantly decreased viability and migration of both B19V-VP1u-treated U937 and THP-1 macrophages are detected in the presence of celastrol. Significantly increased MMP9 activity and elevated NF-kB, MMP9, IL-6, TNF-α, and IL-1β expressions were detected in both B19V-VP1u-treated U937 and THP-1 macrophages. Conversely, celastrol revealed an inhibitory effect on these molecules. Notably, celastrol intervened in this pathogenic process by suppressing the sPLA2 activity of B19V-VP1u and subsequently reducing the inflammatory response. Notably, the administration of B19V-VP1u exacerbated BLE-induced skin fibrosis in mice, with augmented expressions of TGF-β, IL-6, IL-17A, IL-18, and TNF-α, ultimately leading to α-SMA and collagen I deposits in the dermal regions of BLE-induced SSc mice. Altogether, this study sheds light on parvovirus B19 VP1u linked to scleroderma and aggravated dermal fibrosis. Full article
(This article belongs to the Special Issue Molecular Aspects of Autoimmune Diseases)
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8 pages, 2164 KiB  
Communication
Influence of Pre-Analytic Conditions on Quantity of Lymphocytes
by Undine Proschmann, Puya Shalchi Amirkhiz, Pauline Andres, Rocco Haase, Hernan Inojosa, Tjalf Ziemssen and Katja Akgün
Int. J. Mol. Sci. 2023, 24(17), 13479; https://doi.org/10.3390/ijms241713479 - 30 Aug 2023
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Abstract
Lymphocytes are key players in the pathogenesis of multiple sclerosis and a distinct target of several immunomodulatory treatment strategies. In this study, we aim to evaluate the effect of various pre-analytic conditions on immune cell counts to conclude the relevance for clinical implications. [...] Read more.
Lymphocytes are key players in the pathogenesis of multiple sclerosis and a distinct target of several immunomodulatory treatment strategies. In this study, we aim to evaluate the effect of various pre-analytic conditions on immune cell counts to conclude the relevance for clinical implications. Twenty healthy donors were assessed for the effects of distinct storage temperatures and times after blood draws, different durations of tourniquet application, body positions and varying aspiration forces during blood draws. Immune cell frequencies were analyzed using multicolor flowcytometry. While storage for 24 h at 37 °C after blood draws was associated with significantly lower cell counts, different durations of tourniquet application, body positions and varying aspirations speeds did not have significant impacts on the immune cell counts. Our data suggest that immune cell counts are differently affected by pre-analytic conditions being more sensitive to storage temperature. Pre-analytic conditions should be carefully considered when interpreting the laboratory values of immune cell subpopulations. Full article
(This article belongs to the Special Issue Molecular Aspects of Autoimmune Diseases)
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14 pages, 488 KiB  
Article
Mucosal Immune Defence Gene Polymorphisms as Relevant Players in the Pathogenesis of IgA Vasculitis?
by Joao Carlos Batista-Liz, Vanesa Calvo-Río, María Sebastián Mora-Gil, Belén Sevilla-Pérez, Ana Márquez, María Teresa Leonardo, Ana Peñalba, Francisco David Carmona, Javier Narvaez, Luis Martín-Penagos, Lara Belmar-Vega, Cristina Gómez-Fernández, Luis Caminal-Montero, Paz Collado, Patricia Quiroga-Colina, Miren Uriarte-Ecenarro, Esteban Rubio, Manuel León Luque, Juan María Blanco-Madrigal, Eva Galíndez-Agirregoikoa, Javier Martín, Santos Castañeda, Miguel Angel González-Gay, Ricardo Blanco, Verónica Pulito-Cueto and Raquel López-Mejíasadd Show full author list remove Hide full author list
Int. J. Mol. Sci. 2023, 24(17), 13063; https://doi.org/10.3390/ijms241713063 - 22 Aug 2023
Cited by 1 | Viewed by 1430
Abstract
ITGAM–ITGAX (rs11150612, rs11574637), VAV3 rs17019602, CARD9 rs4077515, DEFA (rs2738048, rs10086568), and HORMAD2 rs2412971 are mucosal immune defence polymorphisms, that have an impact on IgA production, described as risk loci for IgA nephropathy (IgAN). Since IgAN and Immunoglobulin-A vasculitis (IgAV) share molecular mechanisms, with [...] Read more.
ITGAM–ITGAX (rs11150612, rs11574637), VAV3 rs17019602, CARD9 rs4077515, DEFA (rs2738048, rs10086568), and HORMAD2 rs2412971 are mucosal immune defence polymorphisms, that have an impact on IgA production, described as risk loci for IgA nephropathy (IgAN). Since IgAN and Immunoglobulin-A vasculitis (IgAV) share molecular mechanisms, with the aberrant deposit of IgA1 being the main pathophysiologic feature of both entities, we assessed the potential influence of the seven abovementioned polymorphisms on IgAV pathogenesis. These seven variants were genotyped in 381 Caucasian IgAV patients and 997 matched healthy controls. No statistically significant differences were observed in the genotype and allele frequencies of these seven polymorphisms when the whole cohort of IgAV patients and those with nephritis were compared to controls. Similar genotype and allele frequencies of all polymorphisms were disclosed when IgAV patients were stratified according to the age at disease onset or the presence/absence of gastrointestinal or renal manifestations. Likewise, no ITGAM–ITGAX and DEFA haplotype differences were observed when the whole cohort of IgAV patients, along with those with nephritis and controls, as well as IgAV patients, stratified according to the abovementioned clinical characteristics, were compared. Our results suggest that mucosal immune defence polymorphisms do not represent novel genetic risk factors for IgAV pathogenesis. Full article
(This article belongs to the Special Issue Molecular Aspects of Autoimmune Diseases)
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