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.

scholarly journals INFECTIONS AND FOLLICULAR LYMPHOMA: IS THERE A LINK?

2017 ◽  
Vol 9 (1) ◽  
pp. e2017035
Author(s):  
Francesco Zallio ◽  
Giulia Limberti ◽  
Marco Ladetto
Keyword(s):  
Follicular Lymphoma ◽  
B Cell ◽  
Bacterial Infections ◽  
Classical Model ◽  
Infectious Agent ◽  
Epidemiological Studies ◽  
Gastric Malt Lymphoma ◽  
Infectious Agents ◽  
Non Hodgkin Lymphoma ◽  
Treatment And Prevention

Several infectious agents appear to provide a proliferative signal -- “antigen-drive” – that  could be implicated in the pathogenesis of various type of Non-Hodgkin Lymphoma (NHL). A classical model of infection-driven lymphoprolipherative disorder is Helicobacter pylori-induced gastric MALT lymphoma, where antibiotic therapy allows eradication of both the infectious agent and the clonal B-cell expansion;  following the footsteps of these example, several retrospective studies have found a correlation with other pathogens and B-cell Lymphomas, adding new important informations about pathogenesis and laying the groundwork for chemotherapy-free treatments.Although no clear association with infectious agents has yet been identified for Follicular Lymphoma (FL), a growing number of biological and clinical observations suggests that interaction with physiological and pathological microbial populations might play a role also in this subtype of lymphoma: in the last years epidemiological studies investigating the association of known risk factors and FL found a potential correlation with viral or bacterial infections; moreover recent findings about the stimulation of FL clones support the importance of microbial exposure to lymphomagenesis and disease progression.In the following review we make an attempt to find tangible evidences in favor of a role of either physiological and pathological exogenous microbial species in the pathogenesis of FL, and try to integrate the findings coming from epidemiological, biological and interventional studies to define future  novel treatment and prevention strategies for FL.

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. 

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 Familial Aggregation of Psoriasis and Co-Aggregation of Autoimmune Diseases in Affected Families

2019 ◽  
Vol 8 (1) ◽  
pp. 115 ◽  
Author(s):  
Yu-Huei Huang ◽  
Chang-Fu Kuo ◽  
Lu-Hsiang Huang ◽  
Mei-Yun Hsieh
Keyword(s):  
Autoimmune Diseases ◽  
Genetic Factors ◽  
Familial Aggregation ◽  
Population Based ◽  
Study Cohort ◽  
Genetic Contribution ◽  
Degree Relative ◽  
Nationwide Study ◽  
Relative Risks ◽  
History Of

Psoriasis is considered to result from the interaction of genetic factors and environmental exposure. The evidence for familial aggregation in psoriasis has been reported but population-based studies related to the magnitude of genetic contribution to psoriasis are rare. This study aimed to evaluate the relative risks of psoriasis in individuals with affected relatives and to calculate the proportion of genetic, shared, and non-shared environmental factors contributing to psoriasis. The study cohort included 69,828 patients diagnosed with psoriasis enrolled in National health Insurance in 2010. The adjusted relative risks (RR) for individuals with an affected first-degree relative and affected second-degree relative were 5.50 (95% CI (Confidence Interval), 5.19–5.82) and 2.54 (95% CI, 2.08–3.12) respectively. For those who have affected first-degree relatives, their RR was 1.45 (95% CI, 1.17–1.79) for Sjogren’s syndrome and 1.94 (95% CI, 1.15–3.27) for systemic sclerosis. This nationwide study ascertains that family history of psoriasis is a risk factor for psoriasis. Individuals with relatives affected by psoriasis have higher risks of developing some autoimmune diseases.

scholarly journals Mechanisms of the induction of autoimmunity

2005 ◽  
Vol 133 (Suppl. 1) ◽  
pp. 9-15 ◽  
Author(s):  
Marija Mostarica-Stojkovic
Keyword(s):  
Immune System ◽  
T Cell ◽  
Autoimmune Diseases ◽  
Molecular Mimicry ◽  
The Body ◽  
Peripheral Tolerance ◽  
High Avidity ◽  
Main Function ◽  
Clonal Deletion ◽  
Genetic Traits

The main function of the immune system is to protect the body by responding to invading microorganisms. Immunologic tolerance is the basic property of the immune system that provides for self/non-self discrimination so that the immune system can protect the host from external pathogens without reacting against itself. Central tolerance is achieved by the clonal deletion of self-reactive lymphocytes expressing receptors with high avidity for self. Autoreactive lymphocytes which escaped selection in the central lymphoid organs are present in the peripheral repertoire but but are kept under control by multiple diverse peripheral tolerance mechanisms acting either directly on the self-reactive T cell (T-cell intrinsic) or indirectly via additional cells (T-cell extrinsic). Intrinsic mec hanisms include ignorance of autoantigens, anergy, phenotype skewing or activation-induced cell death of autoreactive T lymphocytes, while extrinsic mechanisms act through immature and/ or tolerogenic dendritic cells as well as different types of regulatory cells. Autoimmune diseases are associated with humoral or cell-mediated immune reactions against one or more of the body?s own constituents. Activation and clonal expansion of autoreactive lymhocytes is a crucial step in the pathogenesis of autoimmune diseases. They result from the complex interactions between genetic traits and environmental factors, among which infections are the most likely cause. Several basic mechanisms may be operating whereby an infectious agent actually induces apparent autoimmne reactivity including molecular mimicry, bystander activation, induction of costimulation, polyclonal activation, altered processing and expression of cryptic antigens. Although many questions regarding autotolerance and etiop athogenestis of autoimmunity have yet to be resolved, it is evident that multiple overlapping pathways are operative in establishing, maintaining and breaking autotolerance, as well as during the initiation, progression, and final effector phases of autoimmunity.

scholarly journals Zika E Glycan Loop Region and Guillain-Barré Syndrome-Related Proteins: A Possible Molecular Mimicry to be Taken in Account for Vaccine Development

2021 ◽  
Author(s):  
Lebeau Grégorie ◽  
Frumence Etienne ◽  
Turpin Jonathan ◽  
Hoarau Jean-jacques ◽  
Gadea Gilles ◽  
...  
Keyword(s):  
Autoimmune Diseases ◽  
Vaccine Development ◽  
Molecular Mimicry ◽  
In Silico Analysis ◽  
Neurological Complications ◽  
Viral Envelope ◽  
Loop Region ◽  
E Protein ◽  
Voltage Dependent ◽  
Related Proteins

Neurological complications of infection by the mosquito-borne Zika virus (ZIKV) include Guillain-Barré syndrome (GBS), an acute inflammatory demyelinating polyneuritis. GBS was first associated with recent ZIKV epidemics caused by the emergence of ZIKV Asian lineage in South Pacific. Here, we hypothesize that ZIKV-associated GBS relates to a molecular mimicry between viral envelope E (E) protein and neural proteins involved in GBS. Analysis of ZIKV epidemic strains showed that glycan loop (GL) region of the E protein includes an IVNDT motif which is conserved in voltage-dependent L-type calcium channel subunit alpha-1C (Cav1.2) and Heat Shock 70 kDa protein 12A (HSP70 12A). Both VSCC-alpha 1C and HSP70 12A belong to protein families which have been associated with neurological autoimmune diseases in central nervous system. The purpose of our in silico analysis is to point out that IVNDT motif of ZIKV E-GL region should be taken in consideration for the development of safe and effective anti-Zika vaccines by precluding the possibility of adverse neurologic events including autoimmune diseases such as GBS.

Abstract P238: Remission/Cure of Autoimmune Diseases by a Lectin Limite Diet Supplemented With Probiotics, Prebiotics, and Polyphenols

Circulation ◽  
2018 ◽  
Vol 137 (suppl_1) ◽  
Author(s):  
Steven R Gundry
Keyword(s):  
Autoimmune Disease ◽  
Autoimmune Diseases ◽  
Disease Activity ◽  
Immune Cell ◽  
Molecular Mimicry ◽  
Intestinal Barrier ◽  
Signs And Symptoms ◽  
Omega 3 ◽  
Dietary Lectins ◽  
Limited Diet

All autoimmune diseases are highly associated with increased rates of coronary artery and vascular disease secondary to immune cell attack on epithelial cells. The causes of autoimmune disease (AID) seem to be multifactorial. However, the idea that derangement of the microbiome, breaches of the intestinal barrier (leaky gut) and introduction into the human diet of plant defense molecules such as lectins, which are capable of molecular mimicry, prompted our group to investigate the application of a lectin limited diet, coupled with probiotics and prebiotics (The Pant Paradox Protocol) to impact biomarker proven autoimmune disease activity in humans and their impact on endothelial biomarkers of inflammation. One hundred and two consecutive patients with immunoassay markers of autoimmune disease activity, i.e., RF, anti-CCP, ANA, Histone, etc, and signs and symptoms of RA, Lupus, Sjogrens, Crohns, Colitis, Scleroderma, Mixed Connective Tissue Disease, and biomarkers of endothelial inflammation, were enrolled into a program of elimination of major dietary lectins, consisting of all grains and pseudo grains, beans and legumes, peanuts, cashews, nightshades, squashes, and Casein A1 milk products (The Plant Paradox Program), supplemented with probiotics and prebiotics including resistant starches and polyphenol supplements. All pts initially low Vit D levels and low Omega 3 index and adiponectin levels above 16mg/dl. Biomarkers of inflammation, hs-CRP, TNF-alpha, IL-6, fibrinogen, myeloperoxidase and autoimmune markers were measured every 3 months. 95/102 patients achieved complete resolution of autoimmune markers and inflammatory markers within 9 months. The other 7/102 patients all had reduced markers, but incomplete resolution. 80/102 patients were weaned from all immunosuppressive and/or biologic medications without rebound. We conclude that a lectin limited diet, supplemented with pro and prebiotics, and polyphenols are capable of curing or putting into remission most autoimmune diseases.

scholarly journals UVEOGENE: An SNP database for investigations on genetic factors associated with uveitis and their relationship with other systemic autoimmune diseases

2019 ◽  
Vol 40 (3) ◽  
pp. 258-266 ◽  
Author(s):  
Qingfeng Wang ◽  
Guannan Su ◽  
Xiao Tan ◽  
Jing Deng ◽  
Liping Du ◽  
...  
Keyword(s):  
Autoimmune Diseases ◽  
Genetic Factors ◽  
Systemic Autoimmune Diseases ◽  
Factors Associated

scholarly journals The Causal Relationship between Eating Animals and Viral Epidemics

2020 ◽  
Vol 30 (1-6) ◽  
pp. 2-8
Author(s):  
Bhaskara L. Reddy ◽  
Milton H., Jr. Saier
Keyword(s):  
Endangered Species ◽  
Causal Relationship ◽  
Plant Virus ◽  
Prion Diseases ◽  
Infectious Agent ◽  
Vegetarian Diet ◽  
Infectious Agents ◽  
Host Organism ◽  
Animal Host ◽  
Relative Ease

For decades it has been known that infectious agents including pathogenic protozoans, bacteria, and viruses, adapted to a particular animal host, can mutate to gain the ability to infect another host, and the mechanisms involved have been studied in great detail. Although an infectious agent in one animal can alter its host range with relative ease, no example of a plant virus changing its host organism to an animal has been documented. One prevalent pathway for the transmission of infectious agents between hosts involves ingestion of the flesh of one organism by another. In this article we document numerous examples of viral and prion diseases transmitted by eating animals. We suggest that the occurrence of cross-species viral epidemics can be substantially reduced by shifting to a more vegetarian diet and enforcing stricter laws that ban the slaughter and trade of wild and endangered species.

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