Antibodies to histones in infectious mononucleosis

Garzelli, Carlo; Manunta, Maria; Incaprera, Marina; Bazzichi, Agostino; Conaldi, Pier Giulio; Falcone, Giuseppe

doi:10.1016/0165-2478(92)90102-t

Cited by 12 publications

(5 citation statements)

References 15 publications

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“…A main new issue in autoimmunity related to SLE and LN is the definition of specificity of autoantibodies correlated with the disease. In fact, as already discussed in the section on generation mechanisms of anti-dsDNA antibodies, it is possible that anti-dsDNA and anti-Histone form in response to infectious triggers; mononucleosis is an example [95]. Recent evolutions about the characterization of anti-dsDNA and anti-histone antibodies eluted from glomeruli of patient with LN demonstrated that IgG2 was the predominant isotype [56,57]; for their intra-glomerular localization, anti-dsDNA, anti-H2A, and anti-H3 IgG2 were defined as nephritogenic antibodies.…”

Section: Isotype Specificity Of Nephritogenic Anti-dsdna and Anti-mentioning

confidence: 99%

An Update on Antibodies to Necleosome Components as Biomarkers of Sistemic Lupus Erythematosus and of Lupus Flares

Ghiggeri

D’Alessandro

Bartolomeo

et al. 2019

IJMS

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Systemic lupus erythematosus (SLE) is an autoimmune disease with variable clinical expression. It is a potentially devastating condition affecting mostly women and leading to clinically unpredictable outcomes. Remission and flares may, in fact, alternate over time and a mild involvement limited to few articular sites may be followed by severe and widespread organ damage. SLE is the prototype of any autoimmune condition and has, for this reason, attracted the interest of basic immunologists. Therapies have evolved over time and clinical prognosis has, in parallel, been improved. What clinicians still lack is the possibility to use biomarkers of the disease as predictors of outcome and, in this area, several studies are trying to find solutions. Circulating autoantibodies are clearly a milestone of clinical research and the concrete possibility is to integrate, in the future, classical markers of activation (like C3) with target organ autoantibodies. Anti-dsDNA antibodies represent a basic point in any predictive attempt in SLE and should be considered the benchmark for any innovative proposal in the wide field of target organ pathologies related to SLE. DNA is part of the nucleosome that is the basic unit of chromatin. It consists of DNA wrapped around a histone octamer made of 2 copies each of Histone 2A, 2B, 3, and 4. The nucleosome has a plastic organization that varies over time and has the potential to stimulate the formation of antibodies directed to the whole structure (anti-nucleosome) or its parts (anti-dsDNA and anti-Histones). Here, we present an updated review of the literature on antibodies directed to the nucleosome and the nucleosome constituents, i.e., DNA and Histones. Wetriedto merge the data first published more than twenty years ago with more recent results to create a balanced bridge between old dogma and more recent research that could serve as a stimulus to reconsider mechanisms for SLE. The formation of large networks would provide the chance of studying large cohorts of patients and confirm what already presented in small sample size during the last years.

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Section: Isotype Specificity Of Nephritogenic Anti-dsdna and Anti-mentioning

confidence: 99%

An Update on Antibodies to Necleosome Components as Biomarkers of Sistemic Lupus Erythematosus and of Lupus Flares

Ghiggeri

D’Alessandro

Bartolomeo

et al. 2019

IJMS

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“…EBV has the ability to persist in the host as a latent infection that occasionally reactivates, which presumably contributes to the disease flares observed in the chronic SADs. EBV-induced IM has similar symptoms and clinical manifestations as the individual SADs, including presence of rheumatoid factor and other autoantibodies [32, 97–99], and primary acute EBV infection is also known to induce production of nuclear autoantibodies characteristic of SADs [100]. Furthermore, inoculated EBV infection in humanized mice has been demonstrated to generate RA-resembling arthritis [101].…”

Section: Genetic Factors and Possible Mechanisms Associated With Imentioning

confidence: 99%

Epstein-Barr Virus in Systemic Autoimmune Diseases

Draborg

Duus

Houen

2013

Clinical and Developmental Immunology

195

144

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Systemic autoimmune diseases (SADs) are a group of connective tissue diseases with diverse, yet overlapping, symptoms and autoantibody development. The etiology behind SADs is not fully elucidated, but a number of genetic and environmental factors are known to influence the incidence of SADs. Recent findings link dysregulation of Epstein-Barr virus (EBV) with SAD development. EBV causes a persistent infection with a tight latency programme in memory B-cells, which enables evasion of the immune defence. A number of immune escape mechanisms and immune-modulating proteins have been described for EBV. These immune modulating functions make EBV a good candidate for initiation of autoimmune diseases and exacerbation of disease progression. This review focuses on systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), and Sjögren's syndrome (SS) and sum up the existing data linking EBV with these diseases including elevated titres of EBV antibodies, reduced T-cell defence against EBV, and elevated EBV viral load. Together, these data suggest that uncontrolled EBV infection can develop diverse autoreactivities in genetic susceptible individuals with different manifestations depending on the genetic background and the site of reactivation.

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“…Most interesting, presence of rheumafactor and autoantibodies against cellular components like DNA, histones, and ribonucleoproteins is found in IM patients as well as in SLE patients [78, 79]. EBV infection may somehow result in both diseases according to the genetic predisposition and the immune response against EBV in the individual.…”

Section: Association Between Ebv Infection and Slementioning

confidence: 99%

Epstein-Barr Virus and Systemic Lupus Erythematosus

Draborg

Duus

Houen

2012

Clinical and Developmental Immunology

117

111

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The etiology of SLE is not fully established. SLE is a disease with periods of waning disease activity and intermittent flares. This fits well in theory to a latent virus infection, which occasionally switches to lytic cycle, and EBV infection has for long been suspected to be involved. This paper reviews EBV immunobiology and how this is related to SLE pathogenesis by illustrating uncontrolled reactivation of EBV as a disease mechanism for SLE. Studies on EBV in SLE patients show enlarged viral load, abnormal expression of viral lytic genes, impaired EBV-specific T-cell response, and increased levels of EBV-directed antibodies. These results suggest a role for reactivation of EBV infection in SLE. The increased level of EBV antibodies especially comprises an elevated titre of IgA antibodies, and the total number of EBV-reacting antibody isotypes is also enlarged. As EBV is known to be controlled by cell-mediated immunity, the reduced EBV-specific T-cell response in SLE patients may result in defective control of EBV causing frequent reactivation and expression of lytic cycle antigens. This gives rise to enhanced apoptosis and amplified cellular waste load resulting in activation of an immune response and development of EBV-directed antibodies and autoantibodies to cellular antigens.

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Antibodies to histones in infectious mononucleosis

Cited by 12 publications

References 15 publications

An Update on Antibodies to Necleosome Components as Biomarkers of Sistemic Lupus Erythematosus and of Lupus Flares

An Update on Antibodies to Necleosome Components as Biomarkers of Sistemic Lupus Erythematosus and of Lupus Flares

Epstein-Barr Virus in Systemic Autoimmune Diseases

Epstein-Barr Virus and Systemic Lupus Erythematosus

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