Special Issue "Molecular Basis of Autoimmunity Diseases"

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Pathology".

Deadline for manuscript submissions: 31 December 2019.

Special Issue Editor

Prof. Song Guo Zheng
E-Mail Website
Guest Editor
Ranold L. Whisler Chair in Rheumatology and Immunology, Director, Immunology and Rheumatology Research , Ohio State University College of Medicine and Wexner Medical Center, 480 Medical Center Dr. Columbus, OH 43201, USA
Interests: autoimmune diseases; cytokines; T cells; B cells; immune tolerance; cell therapy; antibodies

Special Issue Information

Dear Colleagues,

As you know, the current state-of-the-art treatment of autoimmune diseases is not curative and is associated with considerable toxicity. The major obstacle is that we still lack clear understanding of the molecular basis of the pathogenesis and development of autoimmune diseases. Nonetheless, over the last few years, many studies have been emerging to gain insight into the roles of cells, cytokines, autoantibodies, biomolecules, and genes in initiating and promoting the onset and progression of autoimmune diseases. More importantly, the developed knowledge and approaches have been associated with clinical relevance.

It is my great pleasure to invite you and your teams, as experts from diverse backgrounds (medicine, immunology, clinics, genetics, molecular biology, and epidemiology), as well as those working in the rheumatology and allergic diseases field, to contribute original research or review articles. We are especially interested in articles that cover studies on the identification, roles, and molecular mechanisms of biomolecules and translational approaches of clinical relevance in autoimmune and allergic diseases.

Prof. Song Guo Zheng
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 papers will be 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. Biomolecules is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1200 CHF (Swiss Francs). 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

  • autoimmune diseases
  • biomolecules
  • pathogenesis
  • molecular basis
  • new therapy
  • cytokine
  • cells, T, B, Macrophage, NK, DC and Treg cells

Published Papers (4 papers)

Order results
Result details
Select all
Export citation of selected articles as:

Research

Jump to: Review

Open AccessArticle
HLA-G Polymorphisms Are Associated with Non-Segmental Vitiligo among Brazilians
Biomolecules 2019, 9(9), 463; https://doi.org/10.3390/biom9090463 - 09 Sep 2019
Abstract
(1) Background: Vitiligo is characterized by white patches on the skin caused by loss of melanocyte activity or the absence of these cells. The available treatments minimize the symptoms by retarding the process of skin depigmentation or re-pigmenting the affected regions. New studies [...] Read more.
(1) Background: Vitiligo is characterized by white patches on the skin caused by loss of melanocyte activity or the absence of these cells. The available treatments minimize the symptoms by retarding the process of skin depigmentation or re-pigmenting the affected regions. New studies are required for a better comprehension of the mechanisms that trigger the disease and for the development of more efficient treatments. Studies have suggested an autoimmune feature for vitiligo, based on the occurrence of other autoimmune diseases in vitiligo patients and their relatives, and on the involvement of genes related to the immune response. (2) Methods: We evaluated, by massive parallel sequencing, polymorphisms of the HLA-G gene in vitiligo patients and control samples, to verify if variants of this gene could influence the susceptibility to vitiligo. (3) Results: We detected an association with non-segmental vitiligo regarding the haplotype Distal-010101a/G*01:01:01:01/UTR-1, adjusting for population stratification by using ancestry-informative markers (AIMs). (4) Conclusions: It remains unclear whether the HLA-G variants associated with vitiligo were detected because of the high linkage disequilibrium (LD) with HLA-A*02, or if the HLA-A variants previously reported as associated with vitiligo were detected because of the high LD with HLA-G*01:01:01:01/UTR-1, or if both genes jointly contribute to vitiligo susceptibility. Full article
(This article belongs to the Special Issue Molecular Basis of Autoimmunity Diseases)
Show Figures

Figure 1

Open AccessArticle
Differential Plasma Expression Profiles of Long Non-Coding RNAs Reveal Potential Biomarkers for Systemic Lupus Erythematosus
Biomolecules 2019, 9(6), 206; https://doi.org/10.3390/biom9060206 - 28 May 2019
Cited by 4
Abstract
Identify long non-coding RNAs (lncRNAs) that might serve as biomarkers for systemic lupus erythematosus (SLE) and explore the biological functions of the identified lncRNAs. In the screening phase, we examined the lncRNA expression profile of plasma samples from 24 patients with SLE and [...] Read more.
Identify long non-coding RNAs (lncRNAs) that might serve as biomarkers for systemic lupus erythematosus (SLE) and explore the biological functions of the identified lncRNAs. In the screening phase, we examined the lncRNA expression profile of plasma samples from 24 patients with SLE and 12 healthy controls (HCs) using lncRNA microarray with pooled samples. The candidate lncRNAs were verified in individual samples by quantitative real-time (qRT)-PCR. In the independent validation stage, the identified lncRNAs were evaluated in 240 patients with SLE and 120 HCs. The identified lncRNAs were assessed further in an external validation stage including patients with rheumatoid arthritis (RA) and primary Sjögren’s syndrome (pSS). In addition, we constructed correlated expression networks including coding–non-coding co-expression and competing endogenous RNAs (ceRNAs). Plasma levels of linc0597, lnc0640, and lnc5150 were elevated in SLE patients compared with those of HCs, whereas levels of GAS5 and lnc7074 were decreased. Five lncRNAs were identified as potential SLE biomarkers with an area under the receiver operating characteristic curve (AUC) ranging from 0.604 to 0.833 in the independent validation phase. This panel of five lncRNAs had high diagnostic accuracy for SLE (AUC = 0.966) and distinguished SLE from RA and pSS (AUC = 0.683 and 0.910, respectively). Co-expression analysis showed that GAS5, lnc0640, and lnc5150 may participate in the SLE pathogenesis through the MAPK pathway. The ceRNA network indicated that GAS5, lnc0640, lnc3643, lnc6655, and lnc7074 bind competitively with microRNAs regulating the expression of target genes. Aberrant expression and related pathways suggest the important role of lncRNAs in SLE pathogenesis. In addition, the panel of five lncRNAs (GAS5, lnc7074, linc0597, lnc0640, and lnc5150) in plasma could be used as SLE biomarkers. Full article
(This article belongs to the Special Issue Molecular Basis of Autoimmunity Diseases)
Show Figures

Figure 1

Open AccessArticle
Association between Interleukin 35 Gene Single Nucleotide Polymorphisms and Systemic Lupus Erythematosus in a Chinese Han Population
Biomolecules 2019, 9(4), 157; https://doi.org/10.3390/biom9040157 - 22 Apr 2019
Cited by 2
Abstract
Interleukin-35 (IL-35) exerts crucial roles in the pathogenesis and development of systemic lupus erythematosus (SLE), in this study we aim to explore the associations between IL-35 gene polymorphisms and the susceptibility, clinical features and plasma IL-35 levels of SLE patients, respectively. 490 SLE [...] Read more.
Interleukin-35 (IL-35) exerts crucial roles in the pathogenesis and development of systemic lupus erythematosus (SLE), in this study we aim to explore the associations between IL-35 gene polymorphisms and the susceptibility, clinical features and plasma IL-35 levels of SLE patients, respectively. 490 SLE patients and 489 healthy controls were recruited in our study. The correlations between the polymorphisms of seven SNPs of IL-35 encoding gene and the susceptibility, main clinical manifestations of SLE were evaluated, respectively. Plasma IL-35 levels were assessed in 76 SLE patients, and the associations between plasma IL-35 levels and the polymorphisms of genotyped SNPs were explored. There were significant associations between the polymorphisms of rs4740 and the occurrence of renal disorder, hematological disorder in SLE patients, respectively (p = 0.001; p = 0.001). In addition, there were no significant associations observed between the genotype frequencies of genotyped SNPs and the risk of SLE, plasma IL-35 levels, respectively. The polymorphism of rs4740 of IL-35 encoding gene is associated with the occurrence of renal disorder and hematological disorder of SLE patients. Full article
(This article belongs to the Special Issue Molecular Basis of Autoimmunity Diseases)

Review

Jump to: Research

Open AccessReview
Essential Kinases and Transcriptional Regulators and Their Roles in Autoimmunity
Biomolecules 2019, 9(4), 145; https://doi.org/10.3390/biom9040145 - 10 Apr 2019
Cited by 1
Abstract
Kinases and transcriptional regulators are fundamental components of cell signaling that are expressed on many types of immune cells which are involved in secretion of cytokines, cell proliferation, differentiation, and apoptosis. Both play important roles in biological responses in health as well as [...] Read more.
Kinases and transcriptional regulators are fundamental components of cell signaling that are expressed on many types of immune cells which are involved in secretion of cytokines, cell proliferation, differentiation, and apoptosis. Both play important roles in biological responses in health as well as in illnesses such as the autoimmune diseases which comprise at least 80 disorders. These diseases are caused by complex genetic and environmental interactions that lead to a breakage of immunologic tolerance and a disruption of the balance between self-reactive cells and regulatory cells. Kinases or transcriptional regulatory factors often have an abnormal expression in the autoimmune cells that participate in the pathogenesis of autoimmune disease. These abnormally expressed kinases or transcriptional regulators can over-activate the function of self-reactive cells to produce inflammatory cytokines or down-regulate the activity of regulatory cells, thus causing autoimmune diseases. In this review we introduce five kinds of kinase and transcriptional regulator related to autoimmune diseases, namely, members of the Janus kinase (JAK) family (JAK3 and/or tyrosine kinase 2 (TYK2)), fork head box protein 3 (Foxp3), the retinoic acid-related orphan receptor gamma t (RORγt), and T-box expressed in T cells (T-bet) factors. We also provide a mechanistic insight into how these kinases and transcriptional regulators affect the function of the immune cells related to autoimmune diseases, as well as a description of a current drug design targeting these kinases and transcriptional regulators. Understanding their exact role helps offer new therapies for control of the inflammatory responses that could lead to clinical improvement of the autoimmune diseases. Full article
(This article belongs to the Special Issue Molecular Basis of Autoimmunity Diseases)
Show Figures

Figure 1

Back to TopTop