Antiviral antibody responses in patients with renal disease

Wilson, Curtis B.; Dixon, Frank J.; Evans, Alfred S.; Glassock, Richard J.

doi:10.1016/0090-1229(73)90042-1

Cited by 18 publications

(3 citation statements)

References 52 publications

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“…SLE patients showed decreased levels ofantibodies to streptolysin 0 (26) and of natural antibodies to Escherichia coli and Shigella antigens (28). On the other hand, elevated SLE antibody responses were found against penicillin (29), blood group antigens (30), and a variety of viral antigens (31)(32)(33)(34)(35) (37). However, other studies have indicated that the helper T cell and the antigen-reactive, proliferating T cell might not be the same cell (39)(40)(41).…”

Section: Methods Cell Isolations Peripheral Blood Mononuclear Cells mentioning

confidence: 87%

Immune function in systemic lupus erythematosus. Impairment of in vitro T-cell proliferation and in vivo antibody response to exogenous antigen.

Gottlieb¹,

Lahita²,

Chiorazzi³

et al. 1979

J. Clin. Invest.

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A B S T R A C T Peripheral blood mononuclear cells from 46 systemic lupus erythematosus (SLE) patients showed reduced ability to proliferate in vitro in response to the soluble antigen, tetanus toxoid, as compared with 96 normal controls. Special studies of27 untreated SLE patients also revealed significantly decreased blastogenic responses to tetanus toxoid. In both the total and untreated SLE populations, decreased mean tetanus antibody titers also were found as compared with the control population. However, the reduction in antibody titer and blastogenic response was not strictly parallel.

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Section: Methods Cell Isolations Peripheral Blood Mononuclear Cells mentioning

confidence: 87%

Immune function in systemic lupus erythematosus. Impairment of in vitro T-cell proliferation and in vivo antibody response to exogenous antigen.

Gottlieb¹,

Lahita²,

Chiorazzi³

et al. 1979

J. Clin. Invest.

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“…Serological antibody data can also be misleading. In systemic autoimmune diseases, non-specific immune activation may lead to elevations of antiviral antibody titers [ 6 ]. Screening total immunoglobulin titers can be helpful in this regard.…”

Section: Introductionmentioning

confidence: 99%

Viral-associated glomerulopathies in children

Wenderfer

2015

Pediatr Nephrol

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Viral infections associate temporally with the onset of many glomerular diseases, particularly in children. In other cases of glomerulonephritis, when infection is clinically silent, viral syndromes can still be implicated as a trigger. However, strong evidence for viral causality in most glomerular disease is still lacking. While numerous case reports in children document the occurrence of specific forms of glomerular disease after seroconversion to a wide range of viruses, relatively few reports provide pathologic evidence of viral infection associated with glomerular lesions on kidney biopsy. Strong associations between hepatitis viruses and glomerular injury have been acknowledged in adults, but hepatitis C virus appears not to be an etiology in children. In the context of treating glomerular diseases, when diagnosed, the treatment of hepatitis B virus, cytomegalovirus and human immunodeficiency virus in children with membranoproliferative, membranous and collapsing glomerulopathy plays an important role. Otherwise, there is no evidence suggesting that the identification of a viral infection in a child with glomerulopathy should change the management of the infection or the glomerulonephritis. Therefore, additional research into this topic is very much needed.

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“…Studies have been performed on frequencies and levels of anti bodies to different viral antigens in association with systemic lupus erythematosus (16,17,20) as well as in other disorders, where an auto immune reaction has been suggested, such as in human connective tissue disease (26), in chronic liver disease (37), and in certain renal disorder (38). Rather than representing a reminiscence of an etiologic agent such anti bodies may evidence the presence of a hyper reactive state.…”

Section: Introductionmentioning

confidence: 99%

Role of Virus for the Induction of Myasthenia gravis

Cm¹,

Hammarström²,

Berg³

1978

Eur Neurol

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Virus has been suggested as an etiological agent in myasthenia gravis. In this investigation 36 patients with the clinical diagnosis of myasthenia gravis were tested for antibodies against ornithosis, mycoplasma pneumoniae and 16 viral antigens. Rabbits with experimentally induced autoimmune myasthenia gravis were similarly tested. There was no overall correlation to any microorganism, which might have suggested the involvement of a viral infection in the pathogenesis of the disease. Neither was there any difference in incidence of antibodies in female patients carrying the HLA B8 antigen, an antigen which is associated with myasthenia gravis, as compared to HLA B8 negative individuals.

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Antiviral antibody responses in patients with renal disease

Cited by 18 publications

References 52 publications

Immune function in systemic lupus erythematosus. Impairment of in vitro T-cell proliferation and in vivo antibody response to exogenous antigen.

Immune function in systemic lupus erythematosus. Impairment of in vitro T-cell proliferation and in vivo antibody response to exogenous antigen.

Viral-associated glomerulopathies in children

Role of Virus for the Induction of Myasthenia gravis

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