scholarly journals Molecular mechanisms of induction and acceleration of autoimmunity by microorganisms

2021 ◽  
Vol 20 (1) ◽  
pp. 99-113
Author(s):  
E. P. Kiseleva ◽  
K. I. Mikhailopulo ◽  
G. I. Novik ◽  
N. F. Soroka
Keyword(s):  
T Cells ◽  
Autoimmune Diseases ◽  
Molecular Mechanisms ◽  
Molecular Mimicry ◽  
Ecological Factors ◽  
Infectious Agents ◽  
National Academy Of Sciences ◽  
Adjuvant Effect ◽  
Host Infection ◽  
Cryptic Epitopes

Infectious agents are well-known ecological factors inducing/accelerating human autoimmune diseases. Host infection by a pathogen can lead to autoimmunity via multiple mechanisms: molecular mimicry; epitope spreading and presentation of cryptic epitopes of self-antigen owing to lysis of self-tissue by persisting pathogen or immune cells; bystander activation, adjuvant effect of pathogens as a result of non-specific activation of immune system; polyclonal activation of B-cells by chronic infection; activation of T-cells by bacterial superantigens. Infectious agents and nonpathogenic microorganisms can also protect from autoimmune diseases via activation of regulatory T-cells and displacement of balance between two classes of T helper cells in favor of Th2. This study is supported by the Independent Ethics Committee and approved by the Academic Council of the Institute of Bioorganic Сhemistry, National Academy of Sciences of Belarus. 

scholarly journals Viruses and Autoimmunity: A Review on the Potential Interaction and Molecular Mechanisms

Viruses ◽  
2019 ◽  
Vol 11 (8) ◽  
pp. 762 ◽  
Author(s):  
Maria K. Smatti ◽  
Farhan S. Cyprian ◽  
Gheyath K. Nasrallah ◽  
Asmaa A. Al Thani ◽  
Ruba O. Almishal ◽  
...  
Keyword(s):  
Immune Responses ◽  
Autoimmune Diseases ◽  
Lupus Erythematosus ◽  
Influenza A ◽  
Molecular Mechanisms ◽  
Viral Infections ◽  
Molecular Mimicry ◽  
Experimental Studies ◽  
Onset Time ◽  
Protective Effects

For a long time, viruses have been shown to modify the clinical picture of several autoimmune diseases, including type 1 diabetes (T1D), systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), Sjögren’s syndrome (SS), herpetic stromal keratitis (HSK), celiac disease (CD), and multiple sclerosis (MS). Best examples of viral infections that have been proposed to modulate the induction and development of autoimmune diseases are the infections with enteric viruses such as Coxsackie B virus (CVB) and rotavirus, as well as influenza A viruses (IAV), and herpesviruses. Other viruses that have been studied in this context include, measles, mumps, and rubella. Epidemiological studies in humans and experimental studies in animal have shown that viral infections can induce or protect from autoimmunopathologies depending on several factors including genetic background, host-elicited immune responses, type of virus strain, viral load, and the onset time of infection. Still, data delineating the clear mechanistic interaction between the virus and the immune system to induce autoreactivity are scarce. Available data indicate that viral-induced autoimmunity can be activated through multiple mechanisms including molecular mimicry, epitope spreading, bystander activation, and immortalization of infected B cells. Contrarily, the protective effects can be achieved via regulatory immune responses which lead to the suppression of autoimmune phenomena. Therefore, a better understanding of the immune-related molecular processes in virus-induced autoimmunity is warranted. Here we provide an overview of the current understanding of viral-induced autoimmunity and the mechanisms that are associated with this phenomenon.

scholarly journals Immuno-moodulin: a new anxiogenic factor produced by autoimmune-prone T cells

2019 ◽  
Author(s):  
Giuseppa Piras ◽  
Lorenza Rattazzi ◽  
Nikolaos Paschalidis ◽  
Silvia Oggero ◽  
Giulio Berti ◽  
...  
Keyword(s):  
T Cells ◽  
Mental Disorders ◽  
Transgenic Mice ◽  
Autoimmune Diseases ◽  
Neutralizing Antibodies ◽  
Molecular Mechanisms ◽  
Mononuclear Cells ◽  
Annexin A1 ◽  
Obsessive Compulsive ◽  
Co Morbidity

AbstractPatients suffering from autoimmune diseases are more susceptible to mental disorders yet, the existence of specific cellular and molecular mechanisms behind the co-morbidity of these pathologies is far from being fully elucidated. By generating transgenic mice overexpressing Annexin-A1 exclusively in T cells to study its impact in models of autoimmune diseases, we made the unpredicted observation of an increased level of anxiety. Gene microarray of Annexin-A1 CD4+ T cells identified a novel anxiogenic factor, a small protein of approximately 21kDa encoded by the gene 2610019F03Rik which we named Immuno-moodulin. Neutralizing antibodies against Immuno-moodulin reverted the behavioral phenotype of Annexin-A1 transgenic mice and lowered the basal levels of anxiety in wild type mice; moreover, we also found that patients suffering from obsessive compulsive disorders show high levels of Imood in their peripheral mononuclear cells. We thus identify this protein as a novel peripheral determinant that modulates anxiety behavior. Therapies targeting Immuno-moodulin may lead to a new type of treatment for mental disorders through regulation of the functions of the immune system, rather than directly acting on the nervous system.

scholarly journals T helper cell trafficking in autoimmune kidney diseases

2021 ◽  
Author(s):  
Jan-Hendrik Riedel ◽  
Jan-Eric Turner ◽  
Ulf Panzer
Keyword(s):  
Cell Proliferation ◽  
T Cells ◽  
T Cell ◽  
Autoimmune Diseases ◽  
Molecular Mechanisms ◽  
Current Knowledge ◽  
Kidney Diseases ◽  
T Cell Proliferation ◽  
Special Focus ◽  
Peripheral Tissues

AbstractCD4+ T cells are key drivers of autoimmune diseases, including crescentic GN. Many effector mechanisms employed by T cells to mediate renal damage and repair, such as local cytokine production, depend on their presence at the site of inflammation. Therefore, the mechanisms regulating the renal CD4+ T cell infiltrate are of central importance. From a conceptual point of view, there are four distinct factors that can regulate the abundance of T cells in the kidney: (1) T cell infiltration, (2) T cell proliferation, (3) T cell death and (4) T cell retention/egress. While a substantial amount of data on the recruitment of T cells to the kidneys in crescentic GN have accumulated over the last decade, the roles of T cell proliferation and death in the kidney in crescentic GN is less well characterized. However, the findings from the data available so far do not indicate a major role of these processes. More importantly, the molecular mechanisms underlying both egress and retention of T cells from/in peripheral tissues, such as the kidney, are unknown. Here, we review the current knowledge of mechanisms and functions of T cell migration in renal autoimmune diseases with a special focus on chemokines and their receptors.

Molecular mimicry in systemic lupus erythematosus

Lupus ◽  
2009 ◽  
Vol 18 (13) ◽  
pp. 1181-1185 ◽  
Author(s):  
N. Agmon-Levin ◽  
M. Blank ◽  
Z. Paz ◽  
Y. Shoenfeld
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Autoimmune Disease ◽  
Autoimmune Diseases ◽  
Lupus Erythematosus ◽  
Molecular Mimicry ◽  
Current Evidence ◽  
Systemic Autoimmune Disease ◽  
Infectious Agents ◽  
Systemic Lupus ◽  
Pivotal Mechanism

Systemic lupus erythematosus is a multi-systemic autoimmune disease distinguished by the presence of various autoantibodies. Like most autoimmune diseases, systemic lupus erythematosus is believed to be induced by a combination of genetic, immunologic, and environmental factors, mainly infectious agents. Molecular mimicry between an infectious antigen and self-components is implicated as a pivotal mechanism by which autoimmune diseases such as systemic lupus erythematosus are triggered. Here we review the current evidence of molecular mimicry between different infectious agents and systemic lupus erythematosus.

scholarly journals Molecular Mechanisms of T Cells Activation by Dendritic Cells in Autoimmune Diseases

2018 ◽  
Vol 9 ◽  
Author(s):  
Yu Tai ◽  
Qingtong Wang ◽  
Heinrich Korner ◽  
Lingling Zhang ◽  
Wei Wei
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
Autoimmune Diseases ◽  
Molecular Mechanisms

scholarly journals Infectious diseases and autoimmunity

2011 ◽  
Vol 5 (10) ◽  
pp. 679-687 ◽  
Author(s):  
Lucia Gemma Delogu ◽  
Silvia Deidda ◽  
Giuseppe Delitala ◽  
Roberto Manetti
Keyword(s):  
Autoimmune Diseases ◽  
Bacterial Infections ◽  
Genetic Factors ◽  
Molecular Mimicry ◽  
Infectious Agent ◽  
Host Tissue ◽  
Infectious Agents ◽  
Epitope Spreading ◽  
Time Limits ◽  
Adjuvant Effects

Introduction: Autoimmunity occurs when the immune system recognizes and attacks host tissue. In addition to genetic factors, environmental triggers (in particular viruses, bacteria and other infectious pathogens) are thought to play a major role in the development of autoimmune diseases. Methodology: We searched PubMed, Cochrane, and Scopus without time limits for relevant articles. Results: In this review, we (i) describe the ways in which an infectious agent can initiate or exacerbate autoimmunity; (ii) discuss the evidence linking certain infectious agents to autoimmune diseases in humans; and (iii) describe the animal models used to study the link between infection and autoimmunity. Conclusions: Besides genetic predisposition to autoimmunity, viral and bacterial infections are known to be involved in the initiation and promotion of autoimmune diseases. These studies suggest that pathogens can trigger autoimmunity through molecular mimicry and their adjuvant effects during initiation of disease, and can promote autoimmune responses through bystander activation or epitope spreading via inflammation and/or superantigens.

Resolving Molecular Mechanisms of Autoimmune Disease In Primary CD4 T Cells

2019 ◽  
Author(s):  
Christophe Bourges ◽  
Abigail F. Groff ◽  
Oliver S. Burren ◽  
Chiara Gerhardinger ◽  
Kaia Mattioli ◽  
...  
Keyword(s):  
T Cells ◽  
Autoimmune Disease ◽  
Cd4 T Cells ◽  
Molecular Mechanisms

scholarly journals Molecular remission at T cell level in patients with rheumatoid arthritis

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Jun Inamo ◽  
Katsuya Suzuki ◽  
Masaru Takeshita ◽  
Yasushi Kondo ◽  
Yuumi Okuzono ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
T Cells ◽  
T Cell ◽  
Disease Control ◽  
Expression Profiling ◽  
Molecular Mechanisms ◽  
Principal Component ◽  
Cell Level ◽  
Molecular Remission ◽  
Signature Genes

AbstractWhile numerous disease-modifying anti-rheumatic drugs (DMARDs) have brought about a dramatic paradigm shift in the management of rheumatoid arthritis (RA), unmet needs remain, such as the small proportion of patients who achieve drug-free status. The aim of this study was to explore key molecules for remission at the T cell level, which are known to be deeply involved in RA pathogenesis, and investigate the disease course of patients who achieved molecular remission (MR). We enrolled a total of 46 patients with RA and 10 healthy controls (HCs). We performed gene expression profiling and selected remission signature genes in CD4+ T cells and CD8+ T cells from patients with RA using machine learning methods. In addition, we investigated the benefits of achieving MR on disease control. We identified 9 and 23 genes that were associated with clinical remission in CD4+ and CD8+ T cells, respectively. Principal component analysis (PCA) demonstrated that their expression profiling was similar to those in HCs. For the remission signature genes in CD4+ T cells, the PCA result was reproduced using a validation cohort, indicating the robustness of these genes. A trend toward better disease control was observed during 12 months of follow-up in patients treated with tocilizumab in deep MR compared with those in non-deep MR, although the difference was not significant. The current study will promote our understanding of the molecular mechanisms necessary to achieve deep remission during the management of RA.

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