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Life
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New Insights into the Immunopathogenesis and Therapeutics of Rheumatic Diseases
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New Insights into the Immunopathogenesis and Therapeutics of Rheumatic Diseases

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Medical Research".

Deadline for manuscript submissions: closed (15 June 2021) | Viewed by 17007

Special Issue Editors

Prof. Dr. Der Yuan Chen

E-Mail Website
Guest Editor
Rheumatology and Immunology Center, China Medical University Taichung, Taichung, Taiwan 404, China
Interests: ankylosing spondylitis; psoriasis and psoriatic arthritis; gouty arthritis; osteoporosis; rheumatoid arthritis; systemic lupus erythematosus
Dr. Chi-Chien Lin

E-Mail Website
Guest Editor
Institute of Biomedical Science, The iEGG and Animal Biotechnology Center, National Chung-Hsing University, Taichung 402, Taiwan
Interests: Immuno-oncology; autoimmunity; bioactive natural/organic synthetic pharmaceuticals
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Rheumatic diseases, such as arthritis and spondyloarthropathies, are usually chronic and long-term disorders which affect joints, tendons, ligaments, bones, and muscles and can become more severe over time, leading to low quality of life for patients and substantial economic losses. Rheumatoid arthritis (RA), for instance, is the most common form of autoimmune disease, characterized by persistent joint pain, stiffness, and inflammation. The pathogenesis of RA is considered to be related to the aberrant activation of the innate and adaptative immune systems, including abnormal cytokine productions, eventually causing very severe complications. Given that rheumatoid diseases are heavily impacting people’s health conditions, we aim to publish innovative basic or clinical research studies which could swiftly improve our knowledge of the immunopathogenesis of rheumatoid diseases, quickening the development of immune therapeutics against them.

We would like to invite investigators to contribute their original research and review articles on the pathogenesis of and therapeutics for rheumatic diseases. We are particularly interested in articles describing new pathogenic mechanisms or therapeutic methods based on dysregulated immune responses in rheumatic patients or animal models. 

Potential themes relevant to this Special Issue include the following:

  • Recent developments in the pathogenesis of and therapeutics for rheumatic diseases
  • Researches on natural products with immunomodulatory effects on rheumatic diseases
  • Treatment of rheumatic diseases through the correction of the underlying immune dysregulation
  • Researches in the manipulation of cytokine networks as an approach to treating rheumatic diseases
  • Recent discoveries regarding the role of osteoimmunuology in rheumatic diseases, particularly on the crosstalk between immune and bone systems.
  • Differences between diagnostic criteria and classification criteria for rheumatic diseases

Prof. Der Yuan Chen
Prof. Chi-Chien Lin
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. Life 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 2600 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

  • Rheumatic diseases
  • Therapy
  • Immune dysregulation
  • Cytokine
  • Osteoimmunology
  • Diagnosis

Published Papers (7 papers)

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Research

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14 pages, 4802 KiB  
Article
Psoralea corylifolia L. Ameliorates Collagen-Induced Arthritis by Reducing Proinflammatory Cytokines and Upregulating Myeloid-Derived Suppressor Cells
by Fu-Tzu Pai, Cheng-You Lu, Chia-Hsin Lin, John Wang, Ming-Cheng Huang, Chuan-Teng Liu, Ying-Chyi Song, Cheng-Lung Ku and Hung-Rong Yen
Life 2021, 11(6), 587; https://0-doi-org.brum.beds.ac.uk/10.3390/life11060587 - 21 Jun 2021
Cited by 9 | Viewed by 2233
Abstract
Background: Rheumatoid arthritis is an autoimmune disease that may lead to severe complications. The fruit of Psoralea corylifolia L. (PCL) is widely used in traditional Chinese medicine as a well-known herbal treatment for orthopedic diseases. However, there is a lack of studies [...] Read more.
Background: Rheumatoid arthritis is an autoimmune disease that may lead to severe complications. The fruit of Psoralea corylifolia L. (PCL) is widely used in traditional Chinese medicine as a well-known herbal treatment for orthopedic diseases. However, there is a lack of studies of its effects on rheumatoid arthritis. The purpose of the study was to investigate the effects and mechanisms of concentrated herbal granules of PCL on rheumatoid arthritis to provide some insights for future development of new drug for the treatment of rheumatoid arthritis. Methods: We used collagen-induced arthritis (CIA) DBA/1J mice as an experimental model to mimic human rheumatoid arthritis. The mice were immunized with collagen on days 0 and 21 and then orally administered 200 mg/kg/day PCL on days 22–49. Starch was used as a control. The mice were sacrificed on day 50. Clinical phenotypes, joint histopathology, and immunological profiles were measured. Results: Compared to the CIA or CIA + Starch group, the CIA + PCL group had significantly ameliorated clinical severity and decreased paw swelling. Histopathological analysis of the hind paws showed that PCL mitigated the erosion of cartilage and the proliferation of synovial tissues. There were significant differences in the levels of TNF-α, IL-6 and IL-17A, as measured by ELISA, and the percentages of CD4 + IL-17A+, CD4 + TNF-α+, CD4 + IFN-γ+ T cells. Furthermore, we also found that in mice treated with CIA + PCL, the percentage and number of bone marrow-derived suppressor cells (MDSCs; Gr1+ CD11b+) increased significantly. Conclusions: We provided evidence for the potential antiarthritic effects of PCL through the inhibition of inflammation and increase of MDSCs. These findings indicate that PCL may be a promising therapeutic herb for the treatment of rheumatoid arthritis. Full article
(This article belongs to the Special Issue New Insights into the Immunopathogenesis and Therapeutics of Rheumatic Diseases)
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12 pages, 1201 KiB  
Article
CARD8 SNP rs11672725 Identified as a Potential Genetic Variant for Adult-Onset Still’s Disease
by Wei-Ting Hung, Yi-Ming Chen, Shuen-Iu Hung, Hsin-Hua Chen, Ning-Rong Gung, Chia-Wei Hsieh, Kuo-Tung Tang and Der-Yuan Chen
Life 2021, 11(5), 382; https://0-doi-org.brum.beds.ac.uk/10.3390/life11050382 - 23 Apr 2021
Cited by 5 | Viewed by 2090
Abstract
Adult-onset Still’s disease (AOSD), an autoinflammatory disorder, is related to the dysregulation of NLR3-containing a pyrin domain (NLRP3)-inflammasome signaling. We aimed to investigate the associations of genetic polymorphisms of NLRP3-inflammasome signaling with AOSD susceptibility and outcome and to examine their functional property. Fifty-three [...] Read more.
Adult-onset Still’s disease (AOSD), an autoinflammatory disorder, is related to the dysregulation of NLR3-containing a pyrin domain (NLRP3)-inflammasome signaling. We aimed to investigate the associations of genetic polymorphisms of NLRP3-inflammasome signaling with AOSD susceptibility and outcome and to examine their functional property. Fifty-three candidate single-nucleotide polymorphisms (SNPs) involved in NLRP3-inflammasome response were genotyped using Sequenom MassArray on the samples from 66 AOSD patients and 128 healthy controls. The significant SNPs were validated by direct sequencing using a TaqMan SNP analyzer. Serum levels of associated gene products were examined by ELISA. One SNP rs11672725 of CARD8 gene was identified to be significantly associated with AOSD susceptibility by using MassArray and subsequent replication validation (p = 3.57 × 10−7; odds ratio 3.02). Functional assays showed that serum CARD8 levels were significantly lower in AOSD patients (median, 10,524.6 pg/mL) compared to controls (13,964.1 pg/mL, p = 0.005), while levels of caspase-1, IL-1β and IL-18 were significantly higher in patients (107.1 pg/mL, 2.1 pg/mL, and 1495.8 pg/mL, respectively) than those in controls (99.0 pg/mL, 1.0 pg/mL, and 141.4 pg/mL, respectively). Patients carrying rs11672725CC genotype had significantly higher serum caspase-1 and IL-18 levels (121.3 pg/mL and 1748.6 pg/mL) compared to those with CT/TT genotypes (72.6 pg/mL, p = 0.019 and 609.3 pg/mL, p = 0.046). A higher proportion of patients with rs11672725CC genotype had a systemic pattern of disease outcome, which was linked to low CARD8 levels. A novel variant, rs11672725, of the CARD8 gene was identified as a potential genetic risk for AOSD. Patients carrying the rs11672725CC genotype and C allele had low CARD8 levels, and were predisposed to a systemic pattern with an elevated expression of inflammasome signaling. Full article
(This article belongs to the Special Issue New Insights into the Immunopathogenesis and Therapeutics of Rheumatic Diseases)
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17 pages, 5525 KiB  
Article
Regulatory T Cells Fail to Suppress Fast Homeostatic Proliferation In Vitro
by Daniil Shevyrev, Valeriy Tereshchenko, Elena Blinova, Nadezda Knauer, Ekaterina Pashkina, Alexey Sizikov and Vladimir Kozlov
Life 2021, 11(3), 245; https://0-doi-org.brum.beds.ac.uk/10.3390/life11030245 - 16 Mar 2021
Cited by 6 | Viewed by 2485
Abstract
Homeostatic proliferation (HP) is a physiological process that reconstitutes the T cell pool after lymphopenia involving Interleukin-7 and 15 (IL-7 and IL-15), which are the key cytokines regulating the process. However, there is no evidence that these cytokines influence the function of regulatory [...] Read more.
Homeostatic proliferation (HP) is a physiological process that reconstitutes the T cell pool after lymphopenia involving Interleukin-7 and 15 (IL-7 and IL-15), which are the key cytokines regulating the process. However, there is no evidence that these cytokines influence the function of regulatory T cells (Tregs). Since lymphopenia often accompanies autoimmune diseases, we decided to study the functional activity of Tregs stimulated by HP cytokines from patients with rheumatoid arthritis as compared with that of those from healthy donors. Since T cell receptor (TCR) signal strength determines the intensity of HP, we imitated slow HP using IL-7 or IL-15 and fast HP using a combination of IL-7 or IL-15 with anti-CD3 antibodies, cultivating Treg cells with peripheral blood mononuclear cells (PBMCs) at a 1:1 ratio. We used peripheral blood from 14 patients with rheumatoid arthritis and 18 healthy volunteers. We also used anti-CD3 and anti-CD3 + IL-2 stimulation as controls. The suppressive activity of Treg cells was evaluated in each case by the inhibition of the proliferation of CD4+ and CD8+ cells. The phenotype and proliferation of purified CD3+CD4+CD25+CD127lo cells were assessed by flow cytometry. The suppressive activity of the total pool of Tregs did not differ between the rheumatoid arthritis and healthy donors; however, it significantly decreased in conditions close to fast HP when the influence of HP cytokines was accompanied by anti-CD3 stimulation. The Treg proliferation caused by HP cytokines was lower in the rheumatoid arthritis (RA) patients than in the healthy individuals. The revealed decrease in Treg suppressive activity could impact the TCR landscape during lymphopenia and lead to the proliferation of potentially self-reactive T cell clones that are able to receive relatively strong TCR signals. This may be another explanation as to why lymphopenia is associated with the development of autoimmune diseases. The revealed decrease in Treg proliferation under IL-7 and IL-15 exposure can lead to a delay in Treg pool reconstitution in patients with rheumatoid arthritis in the case of lymphopenia. Full article
(This article belongs to the Special Issue New Insights into the Immunopathogenesis and Therapeutics of Rheumatic Diseases)
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12 pages, 482 KiB  
Article
Single Nucleotide Polymorphism in the IL17A Gene Is Associated with Interstitial Lung Disease Positive to Anti-Jo1 Antisynthetase Autoantibodies
by Marco Antonio Ponce-Gallegos, Montserrat I. González-Pérez, Mayra Mejía, Karol J. Nava-Quiroz, Gloria Pérez-Rubio, Ivette Buendía-Roldán, Espiridión Ramos-Martínez, Jorge Rojas-Serrano and Ramcés Falfán-Valencia
Life 2021, 11(2), 174; https://0-doi-org.brum.beds.ac.uk/10.3390/life11020174 - 23 Feb 2021
Viewed by 2668
Abstract
Antisynthetase syndrome (ASSD) is a rare multisystemic connective tissue disease affecting the skin, joints, muscles, and lungs, characterized by anti-aminoacyl transfer-RNA-synthetases (anti-tRNA) autoantibodies production, being anti-Jo1 the most frequent. We included one-hundred twenty-one ASSD patients and 340 healthy subjects (HS), and also, we [...] Read more.
Antisynthetase syndrome (ASSD) is a rare multisystemic connective tissue disease affecting the skin, joints, muscles, and lungs, characterized by anti-aminoacyl transfer-RNA-synthetases (anti-tRNA) autoantibodies production, being anti-Jo1 the most frequent. We included one-hundred twenty-one ASSD patients and 340 healthy subjects (HS), and also, we divided the case group into anti-Jo1 and non-anti-Jo1. Two single nucleotide polymorphisms (SNPs) in the IL17A gene were evaluated. Anti-Jo1 was the most common anti-tRNA antibody in our cohort, and the most frequent tomographic pattern was non-specific interstitial pneumonia (NSIP). Anti-Jo1 ASSD patients had higher levels of creatine phosphokinase than the non-anti-Jo1 group. Significant differences in genotype frequencies with rs8193036/CC between anti-Jo1 vs. non-anti-Jo1 ASSD patients (p < 0.001), maintaining the association after Bonferroni correction (p = 0.002). Additionally, in the anti-Jo1 group vs. HS comparison, we found a statistically significant difference with the same SNP (p = 0.018, OR = 2.91, 95% CI = 1.15–7.35), maintaining the association after Bonferroni correction (p = 0.036). The rs8193036/CC genotype in IL17A is associated with ASSD patients with anti-Jo1. Also, anti-Jo1 and non-anti-Jo1 patients display differences in genotype frequencies. Full article
(This article belongs to the Special Issue New Insights into the Immunopathogenesis and Therapeutics of Rheumatic Diseases)
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15 pages, 2338 KiB  
Article
Association of Apolipoprotein E Polymorphism with Adipokines and Cardiovascular Disease Risk in Rheumatoid Arthritis Patients
by Yi-Ming Chen, Po-Ku Chen, Ching-Kun Chang, Chi-Chen Lin, Hsin-Hua Chen, Joung-Liang Lan, Shih-Hsin Chang and Der-Yuan Chen
Life 2020, 10(12), 330; https://0-doi-org.brum.beds.ac.uk/10.3390/life10120330 - 07 Dec 2020
Cited by 9 | Viewed by 1888
Abstract
Apolipoprotein E (ApoE) polymorphism and adipokines are linked to atherosclerosis. We aimed to investigate the associations of apoE genotypes with adipokines, inflammatory parameters, and cardiovascular disease (CVD) risks in rheumatoid arthritis (RA) patients. We enrolled 152 RA patients and 49 healthy control (HC) [...] Read more.
Apolipoprotein E (ApoE) polymorphism and adipokines are linked to atherosclerosis. We aimed to investigate the associations of apoE genotypes with adipokines, inflammatory parameters, and cardiovascular disease (CVD) risks in rheumatoid arthritis (RA) patients. We enrolled 152 RA patients and 49 healthy control (HC) subjects. The apoE genotyping was determined by a polymerase chain reaction, while plasma levels of adipokines and inflammatory cytokines were measured with ELISA. Although apoE genotypes distributions were indistinguishable between RA patients and HC, we found significantly higher levels of apoE and adipokines in RA patients compared with HC. RA patients with ε2ε3 genotype had lower levels of TNF-α, IL-6, resistin, and visfatin, but higher leptin levels compared with ε3ε3 genotype patients. Patients with ε3ε4 genotype had significantly higher low-density lipoprotein-cholesterol (LDL-C) levels and atherogenic index scores compared with ε2ε3 genotype carriers. Moreover, patients with ε2ε3 genotype had significantly lower 10-year CVD risk than ε3ε3 or ε3ε4 genotype patients. ε3ε4 genotype and adiponectin levels were independent predictors of a high 10-year CVD risk. RA patients with ε2ε3 genotype are associated with lower levels of TNF-α, IL-6, resistin, visfatin, and CVD risk, while RA patients with ε3ε4 genotype exhibited higher levels of LDL-C, insulin resistance, and higher CVD risks. Full article
(This article belongs to the Special Issue New Insights into the Immunopathogenesis and Therapeutics of Rheumatic Diseases)
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17 pages, 2232 KiB  
Article
Aqueous Extract of Kan-Lu-Hsiao-Tu-Tan Ameliorates Collagen-Induced Arthritis in Mice by Inhibiting Oxidative Stress and Inflammatory Responses
by Chih-Chao Chiang, Yi-Rong Li, Kuei-Hung Lai, Wei-Jen Cheng, Shih-Chao Lin, Yi-Hsuan Wang, Po-Jen Chen, Sien-Hung Yang, Chi-Chien Lin and Tsong-Long Hwang
Life 2020, 10(12), 313; https://0-doi-org.brum.beds.ac.uk/10.3390/life10120313 - 27 Nov 2020
Cited by 4 | Viewed by 2446
Abstract
Background: Kan-Lu-Hsiao-Tu-Tan (KLHTT) exhibits anti-psoriatic effects through anti-inflammatory activity in mice. However, the therapeutic effects of KLHTT on rheumatoid arthritis (RA), another significant autoimmune inflammatory disorder, have not been elucidated. Herein, we explored the anti-arthritic effects of KLHTT on collagen-induced arthritis (CIA) in [...] Read more.
Background: Kan-Lu-Hsiao-Tu-Tan (KLHTT) exhibits anti-psoriatic effects through anti-inflammatory activity in mice. However, the therapeutic effects of KLHTT on rheumatoid arthritis (RA), another significant autoimmune inflammatory disorder, have not been elucidated. Herein, we explored the anti-arthritic effects of KLHTT on collagen-induced arthritis (CIA) in mice. Methods: KLHTT was extracted by boiling water and subjected to spectroscopic analysis. Chicken collagen type II (CII) with complete Freund’s adjuvant was intradermally injected to induce CIA in DBA/1J mice. Anti-CII antibody, cytokines, malondialdehyde (MDA), and hydrogen peroxide (H2O2) were measured using ELISA, thiobarbituric acid reactive substances, and a hydrogen peroxide assay kit. Splenocyte proliferation was tested using thymidine incorporation. Th1 and Th17 cells were analyzed by flow cytometry. Results: Oral KLHTT treatment (50 and 100 mg/kg) ameliorated mouse CIA by decreasing the levels of interleukin (IL)-1β, IL-6, IL-17A, and tumour necrosis factor-α in the paw homogenates and serum. KLHTT also suppressed anti-CII antibody formation, splenocyte proliferation, and splenic Th1 and Th17 cell numbers. Additionally, KLHTT showed antioxidant activity by reducing the concentrations of MDA and H2O2 in paw tissues. Conclusions: The therapeutic effects of KLHTT in CIA mice were through regulating oxidative stress and inflammatory responses. Our results suggest that KLHTT has potential to treat RA. Full article
(This article belongs to the Special Issue New Insights into the Immunopathogenesis and Therapeutics of Rheumatic Diseases)
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Review

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11 pages, 705 KiB  
Review
Dendritic Cells and Antiphospholipid Syndrome: An Updated Systematic Review
by Kuo-Tung Tang, Hsin-Hua Chen, Tzu-Ting Chen, Nicole R. Bracci and Chi-Chien Lin
Life 2021, 11(8), 801; https://0-doi-org.brum.beds.ac.uk/10.3390/life11080801 - 09 Aug 2021
Cited by 5 | Viewed by 2456
Abstract
Antiphospholipid syndrome (APS) is an autoimmune disease characterized by autoreactive B and T cells against β2-glycoprotein I (B2GPI), with vascular thrombosis or obstetrical complications. Dendritic cells (DCs) are crucial in the generation of autoimmunity. Here, we conducted a comprehensive systematic review on the [...] Read more.
Antiphospholipid syndrome (APS) is an autoimmune disease characterized by autoreactive B and T cells against β2-glycoprotein I (B2GPI), with vascular thrombosis or obstetrical complications. Dendritic cells (DCs) are crucial in the generation of autoimmunity. Here, we conducted a comprehensive systematic review on the relationship between DC and APS. We performed a literature search of PubMed as of 26 March 2021. A total of 33 articles were extracted. DCs are pivotal in inducing inflammatory responses and orchestrating adaptive immunity. DCs contribute to the local inflammation regarding vascular thrombosis or obstetrical complications. Both B2GPI and antiphospholipid antibodies (aPL) can promote antigen presentation by DCs and the generation or maintenance of autoimmunity. In addition, plasmacytoid DC activation is enhanced by aPL, thereby augmenting the inflammatory response. In line with these findings, DC modulation appears promising as a future treatment for APS. In conclusion, our review indicated the crucial role of DCs in the pathogenesis of APS. Deeper understanding of the complex relationship would help in developing new treatment strategies. Full article
(This article belongs to the Special Issue New Insights into the Immunopathogenesis and Therapeutics of Rheumatic Diseases)
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