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New Insights in Biomarkers of Autoimmune and Autoinflammatory Diseases
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New Insights in Biomarkers of Autoimmune and Autoinflammatory 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: 20 February 2025 | Viewed by 14810

Special Issue Editors

Dr. Mariapaola Marino

E-Mail Website
Guest Editor
1. Dipartimento di Medicina e Chirurgia Traslazionale, Sezione di Patologia Generale, Università Cattolica del Sacro Cuore, 00168 Rome, Italy
2. Fondazione Policlinico Universitario “A. Gemelli” IRCCS, 00168 Rome, Italy
Interests: immunology; autoimmunity; inflammation; biomarkers
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Umberto Basile

E-Mail Website
Guest Editor
Head, Clinical Pathology Unit, Hospital “Santa Maria Goretti” ASL Latina, 04100 Latina, Italy
Interests: autoimmunity; cancer; monoclonal gammopathy; minimal residual disease; biomarkers; other biological fluid; new technologies
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The deregulation of innate and adaptive immune systems affects 5% of the worldwide population with a high impact in terms of clinical impairment, morbidity, and, due to the chronic conditions, a significant economic burden in the long run. Inflammation, the long arm of innate immunity, as a mediator of effects may be involved or deregulated in itself, in absence of an auto-attack of the immune system, paving the way for those conditions included under the umbrella name of autoinflammatory diseases. Accordingly, cellular and molecular biomarkers are largely involved in diagnosis, prognosis, response to therapies, and follow-up, providing a prediction of changes in disease activity. Taking into account the individual and genetic susceptibility as well as the wide range of environment risk factors that concur with the pathogenesis, the importance of research to set-up and validate novel, effective, and personalised biomarkers of autoimmune and autoinflammatory conditions stands alone. This Special Issue is devoted to the most recent results aimed at exploiting the clinical potential of biomarkers measuring the disordered immune response.

Potential topics include, but are not limited to:

  • Innate immunity;
  • Adaptive immunity;
  • Inflammation;
  • Immunoglobulins;
  • Autoantibodies;
  • Free light chains;
  • Peptides;
  • Cytokines;
  • Receptors;
  • Leukocytes;
  • Extracellular vesicles;
  • Signal transduction;
  • Inflammaging;
  • Inflammasome.

Dr. Mariapaola Marino
Dr. Umberto Basile
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. 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

  • inflammaging
  • inflammasome
  • autoantibodies
  • free light chains
  • cytokines
  • receptor
  • signal transduction
  • innate immunity
  • adaptive immunity

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Published Papers (6 papers)

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Research

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12 pages, 2296 KiB  
Article
Anti-TCP1 Antibody Is a Potential Biomarker for Diagnosing Systemic Lupus Erythematosus
by Sang-Won Lee, Wook-Young Baek, So-Won Park, Jee-Min Chung, Ji-Hyun Park, Ho Chul Kang, Ju-Yang Jung and Chang-Hee Suh
Int. J. Mol. Sci. 2024, 25(16), 8612; https://doi.org/10.3390/ijms25168612 - 7 Aug 2024
Viewed by 794
Abstract
Systemic lupus erythematosus (SLE) is a chronic inflammatory disease caused by autoantibodies. Serum samples from patients with SLE (n = 10) were compared with those from normal controls (NCs, n = 5) using 21K protein chip analysis to identify a biomarker for [...] Read more.
Systemic lupus erythematosus (SLE) is a chronic inflammatory disease caused by autoantibodies. Serum samples from patients with SLE (n = 10) were compared with those from normal controls (NCs, n = 5) using 21K protein chip analysis to identify a biomarker for SLE, revealing 63 SLE-specific autoantibodies. The anti-chaperonin-containing t-complex polypeptide-1 (TCP1) antibody exhibited higher expression in patients with SLE than in NCs. To validate the specificity of the anti-TCP1 antibody in SLE, dot blot analysis was conducted using sera from patients with SLE (n = 100), rheumatoid arthritis (RA; n = 25), Behçet’s disease (BD; n = 28), and systemic sclerosis (SSc; n = 30) and NCs (n = 50). The results confirmed the detection of anti-TCP1 antibodies in 79 of 100 patients with SLE, with substantially elevated expression compared to both NCs and patients with other autoimmune diseases. We performed an enzyme-linked immunosorbent assay to determine the relative amounts of anti-TCP1 antibodies; markedly elevated anti-TCP1 antibody levels were detected in the sera of patients with SLE (50.1 ± 17.3 arbitrary unit (AU), n = 251) compared to those in NCs (33.9 ± 9.3 AU), RA (35 ± 8.7 AU), BD (37.5 ± 11.6 AU), and SSc (43 ± 11.9 AU). These data suggest that the anti-TCP1 antibody is a potential diagnostic biomarker for SLE. Full article
(This article belongs to the Special Issue New Insights in Biomarkers of Autoimmune and Autoinflammatory Diseases)
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13 pages, 2200 KiB  
Article
Deletion of the Mitochondrial Membrane Protein Fam210b Is Associated with the Development of Systemic Lupus Erythematosus
by Yaqi Xu, Ran Gao, Min Zhang, Qi Zeng, Gaizhi Zhu, Jinming Qiu, Wenting Su and Renxi Wang
Int. J. Mol. Sci. 2024, 25(13), 7253; https://doi.org/10.3390/ijms25137253 - 1 Jul 2024
Viewed by 3783
Abstract
Mitochondrial dysfunction has been increasingly recognized as a trigger for systemic lupus erythematosus (SLE). Recent bioinformatics studies have suggested Fam210b as a significant candidate for the classification and therapeutic targeting of SLE. To experimentally prove the role of Fam210b in SLE, we constructed [...] Read more.
Mitochondrial dysfunction has been increasingly recognized as a trigger for systemic lupus erythematosus (SLE). Recent bioinformatics studies have suggested Fam210b as a significant candidate for the classification and therapeutic targeting of SLE. To experimentally prove the role of Fam210b in SLE, we constructed Fam210b knockout (Fam210b−/−) mice using the CRISPR-Cas9 method. We found that approximately 15.68% of Fam210b−/− mice spontaneously developed lupus-like autoimmunity, which was characterized by skin ulcerations, splenomegaly, and an increase in anti-double-stranded DNA (anti-dsDNA) IgG antibodies and anti-nuclear antibodies(ANA). Single-cell sequencing showed that Fam210b was mainly expressed in erythroid cells. Critically, the knockout of Fam210b resulted in abnormal erythrocyte differentiation and development in the spleens of mice. Concurrently, the spleens exhibited an increased number of CD71+ erythroid cells, along with elevated levels of reactive oxygen species (ROS) in the erythrocytes. The co-culture of CD71+ erythroid cells and lymphocytes resulted in lymphocyte activation and promoted dsDNA and IgG production. In summary, Fam210b knockout leads to a low probability of lupus-like symptoms in mice through the overproduction of ROS in CD71+ erythroid cells. Thus, Fam210b reduction may serve as a novel key marker that triggers the development of SLE. Full article
(This article belongs to the Special Issue New Insights in Biomarkers of Autoimmune and Autoinflammatory Diseases)
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11 pages, 924 KiB  
Article
The Expression of Toll-like Receptors (TLR7 and TLR9) in Class III and Class IV of Recently Diagnosed Lupus Nephritis with 12-Month Follow-Up
by José Ignacio Cerrillos-Gutiérrez, Miguel Medina-Pérez, Jorge Andrade-Sierra, Andrés García-Sánchez, Ernesto Germán Cardona-Muñoz, Wendy Campos-Pérez, Erika Martínez-López, Daniela Itzel Sánchez-Lozano, Tannia Isabel Campos-Bayardo, Daniel Román-Rojas, Luis Francisco Gómez-Hermosillo, Jorge Casillas-Moreno and Alejandra Guillermina Miranda-Díaz
Int. J. Mol. Sci. 2024, 25(13), 7023; https://doi.org/10.3390/ijms25137023 - 27 Jun 2024
Viewed by 1732
Abstract
Renal involvement is an important cause of morbidity and mortality in systemic lupus erythematosus (SLE). The present study included patients with recently diagnosed Class III and Class IV lupus nephritis (LN) treated by Rheumatology who, upon the detection of alterations in their kidney [...] Read more.
Renal involvement is an important cause of morbidity and mortality in systemic lupus erythematosus (SLE). The present study included patients with recently diagnosed Class III and Class IV lupus nephritis (LN) treated by Rheumatology who, upon the detection of alterations in their kidney function, were referred to Nephrology for the joint management of both medical specialties. The purpose of this study was to compare the plasma expression of Toll-Like Receptor 7 (TLR7) and TLR9 in healthy control (HC) subjects and newly diagnosed Class III and Class IV LN patients with 12-month follow-ups. The plasma expression of TLR7 and TLR9 proteins was determined by the ELISA method. A significant increase in the expression of TLR7 protein was found in Class III LN in the basal determination compared to the expression in the HC (p = 0.002) and at 12 months of follow-up (p = 0.03) vs. HC. The expression of TLR9 showed a behavior opposite to that of TLR7. TLR9 showed decreased protein expression in LN Class III patients’ baseline and final measurements. The result was similar in the basal and final determinations of LN Class IV compared to the expression in HC. A significant decrease in SLEDAI -2K was observed at 12 months of follow-up in patients in Class III (p = 0.01) and Class IV (p = 0.0001) of LN. Complement C3 levels improved significantly at 12-month follow-up in Class IV patients (p = 0.0001). Complement C4 levels decreased significantly at 12-month follow-up in LN Class III compared to baseline (p = 0.01). Anti-DNA antibodies decreased significantly at 12 months of follow-up in Class IV LN (p = 0.01). A significant increase in proteinuria was found at 12 months of follow-up in Class III LN, compared to the baseline determination (p = 0.02). In LN Class IV, proteinuria decreased at 12 months of follow-up compared to baseline (p = 0.0001). Albuminuria decreased at 12 months of follow-up in LN Class IV (p = 0.006). Class IV LN, albuminuria also decreased at 12 months of follow-up (p = 0.009). Hematuria persisted in all patients and the glomerular filtration rate did not change. Three Class IV patients died before 12 months of follow-up from various causes. In conclusion, although the rheumatologic data appeared to improve, the renal function data remained inconsistent. Decreased expression of TLR9 and increased expression of TLR7 could be useful in the early diagnosis of Class III and Class IV LN is correct. Full article
(This article belongs to the Special Issue New Insights in Biomarkers of Autoimmune and Autoinflammatory Diseases)
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Review

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13 pages, 753 KiB  
Review
Role of Interleukin 6 in Acute Pancreatitis: A Possible Marker for Disease Prognosis
by Alexandra Mititelu, Alina Grama, Marius-Cosmin Colceriu, Gabriel Benţa, Mihaela-Simona Popoviciu and Tudor Lucian Pop
Int. J. Mol. Sci. 2024, 25(15), 8283; https://doi.org/10.3390/ijms25158283 - 29 Jul 2024
Viewed by 1018
Abstract
Acute pancreatitis (AP) is a significant cause of morbidity, even in children, and is frequently associated with systemic manifestations. There are many cytokines involved in the inflammatory response characteristic of this disease. Interleukin 6 (IL-6) is one of the most important cytokines involved [...] Read more.
Acute pancreatitis (AP) is a significant cause of morbidity, even in children, and is frequently associated with systemic manifestations. There are many cytokines involved in the inflammatory response characteristic of this disease. Interleukin 6 (IL-6) is one of the most important cytokines involved in AP, beginning from cellular injury and continuing to the systemic inflammatory response and distant organ involvement. IL-6 is a multifunctional cytokine that regulates acute-phase response and inflammation. It is produced by various cells and exerts its biological role on many cells through its high-affinity complex receptor. IL-6 has been investigated as a predicting maker for severe forms of AP. Many studies have validated the use of IL-6 serum levels in the first 48 h as a reliable marker for severe evolution and multisystemic involvement. Still, it has not been used in daily practice until now. This review discusses the main binding mechanisms by which IL-6 triggers cellular response and the AP pathogenetic mechanisms in which IL-6 is involved. We then emphasize the promising role of IL-6 as a prognostic marker, which could be added as a routine marker at admission in children with AP. Full article
(This article belongs to the Special Issue New Insights in Biomarkers of Autoimmune and Autoinflammatory Diseases)
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15 pages, 1843 KiB  
Review
Tumor Necrosis Factor-Alpha: Ally and Enemy in Protean Cutaneous Sceneries
by Krizia Pocino, Valeria Carnazzo, Annunziata Stefanile, Valerio Basile, Cristina Guerriero, Mariapaola Marino, Donato Rigante and Umberto Basile
Int. J. Mol. Sci. 2024, 25(14), 7762; https://doi.org/10.3390/ijms25147762 - 16 Jul 2024
Cited by 1 | Viewed by 1140
Abstract
Skin is the forestage for a series of many-sided functions of tumor necrosis factor-alpha (TNF-α), a proinflammatory cytokine with staggering versatility and sizable implications for tissue homeostasis, immune responses, angiogenesis, apoptosis, local and systemic inflammation. An aberrant TNF-α-mediated crosstalk has been linked to [...] Read more.
Skin is the forestage for a series of many-sided functions of tumor necrosis factor-alpha (TNF-α), a proinflammatory cytokine with staggering versatility and sizable implications for tissue homeostasis, immune responses, angiogenesis, apoptosis, local and systemic inflammation. An aberrant TNF-α-mediated crosstalk has been linked to the pathogenesis of acute and chronic skin inflammatory diseases, and indeed, TNF-α dysregulation can contribute to the development and progression of psoriasis, vitiligo, local damage following exposition to ultraviolet light radiations, cutaneous lupus erythematosus, and acne vulgaris. Therapies that target TNF-α are conspicuously used in the treatment of different skin disorders, aiming to modulate the in vivo immune functions triggered by many cutaneous cells, including keratinocytes, mast cells, or Langerhans cells, and reduce inflammation taking place within the skin. Herein, we focus on the key relationships between TNF-α and distinct skin non-neoplastic inflammatory or physiologic conditions, showing that a natural induction of TNF-α may have a protective significance but that TNF-α overproduction may be harmful or even lethal. Many questions remain unraveled in the therapeutic practice, and caution should be exercised due to eventual backlashes exerted by TNF-α in maintaining skin health or in provoking skin disease. Full article
(This article belongs to the Special Issue New Insights in Biomarkers of Autoimmune and Autoinflammatory Diseases)
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18 pages, 1080 KiB  
Review
Autoimmunity, New Potential Biomarkers and the Thyroid Gland—The Perspective of Hashimoto’s Thyroiditis and Its Treatment
by Ewa Tywanek, Agata Michalak, Joanna Świrska and Agnieszka Zwolak
Int. J. Mol. Sci. 2024, 25(9), 4703; https://doi.org/10.3390/ijms25094703 - 26 Apr 2024
Viewed by 5604
Abstract
Autoimmune thyroid disease (AITD) is the most common organic specific illness of the thyroid gland. It may manifest as the overproduction or the decline of thyroxine and triiodothyronine. Hyperthyroidism develops due to the overproduction of hormones as an answer to the presence of [...] Read more.
Autoimmune thyroid disease (AITD) is the most common organic specific illness of the thyroid gland. It may manifest as the overproduction or the decline of thyroxine and triiodothyronine. Hyperthyroidism develops due to the overproduction of hormones as an answer to the presence of stimulatory antibodies against the TSH receptor. Hashimoto’s thyroiditis (HT) is generally characterized by the presence of thyroid peroxidase and thyroglobulin antibodies, with a concomitant infiltration of lymphocytes in the thyroid. Due to the progressive destruction of cells, AITD can lead to subclinical or overt hypothyroidism. Pathophysiology of AITD is extremely complicated and still not fully understood, with genetic, environmental and epigenetic factors involved in its development. Due to increasing incidence and social awareness of this pathology, there is an urgent need to expand the background concerning AITD. A growing body of evidence suggests possible ways of treatment apart from traditional approaches. Simultaneously, the role of potential new biomarkers in the diagnosis and monitoring of AITD has been highlighted recently, too. Therefore, we decided to review therapeutic trends in the course of AITD based on its pathophysiological mechanisms, mainly focusing on HT. Another aim was to summarize the state of knowledge regarding the role of new biomarkers in this condition. Full article
(This article belongs to the Special Issue New Insights in Biomarkers of Autoimmune and Autoinflammatory Diseases)
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