Anti-endothelial cell antibodies in nephropathia epidemica and other viral diseases

Wangel, A. G.; Temonen, Mari; Brummer-Korvenkontio, M; Vaheri, Antti

doi:10.1111/j.1365-2249.1992.tb05824.x

Cited by 20 publications

(2 citation statements)

References 27 publications

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“…Specifically, the vascular endothelium is a sensitive target of the inflammatory response in several autoimmune diseases including systemic lupus erythematosus and rheumatoid arthritis (10–12). While the endothelium is a dynamic structure involved in tissue homeostasis, luminal inflammation and subsequent dysfunction result in clinically significant end-organ injury.…”

Section: Discussionmentioning

confidence: 99%

Autoimmune-Mediated Vascular Injury Occurs Prior to Sustained Hyperglycemia in a Murine Model of Type I Diabetes Mellitus

Zimmerman¹,

Haskins

Bradley

et al. 2011

Journal of Surgical Research

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Introduction Accelerated cardiovascular disease in patients with type I diabetes (TID) is a well-described condition and serious clinical obstacle. At present, the notion that early atherogenesis is largely dependent on sustained hyperglycemia remains in question. We hypothesize that an alteration in T lymphocyte homeostasis may result in early vascular inflammation which might amplify subsequent blood vessel injury in euglycemia. Methods A murine of carotid arterial ligation was employed to induce neointimal hyperplasia (NIH) in wild type and non-obese diabetic (NOD) mice. Additionally, adoptive transfer of NOD splenocytes into immunodeficient NOD mice (NOD.scid) was undertaken to evaluate the influence of restored autoimmunity on NIH development. Results Interestingly, compared to wild type mice, the NOD demonstrate a significant increase in neointimal area. Conversely, the NOD.scid reveal almost no evidence of vascular injury. While evidence of early vascular inflammation can be detected in the injured NOD vasculature, uninjured contralateral vessels and those of the NOD.scid have minimal T cell infiltration. Following reconstitution of autoimmune responses via NOD splenocyte adoptive transfer, accelerated vascular pathology is restored. Conclusions These observations suggest that autoimmunity, in the setting of impending hyperglycemia, may contribute to accelerated vascular inflammation and subsequent pathology.

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Section: Discussionmentioning

confidence: 99%

Autoimmune-Mediated Vascular Injury Occurs Prior to Sustained Hyperglycemia in a Murine Model of Type I Diabetes Mellitus

Zimmerman¹,

Haskins

Bradley

et al. 2011

Journal of Surgical Research

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show abstract

“…In early studies [ 33 ] we found rheumatoid factors, recognized in viral illnesses, circulating immune complexes, and increased levels of IgM in all 18 patients with PUUV-induced disease; the levels of IgG and IgA increased during the clinical disease but remained normal. We also found anti-endothelial cell antibodies in NE and other viral diseases [ 34 ]. We detected autoimmune polyendocrinopathy and hypophysitis after PUUV infection [ 35 ].…”

Section: Role Of Different Factors In the Variationmentioning

confidence: 93%

Puumala Hantavirus Infections Show Extensive Variation in Clinical Outcome

Vaheri

Smura

Vauhkonen

et al. 2023

Viruses

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The clinical outcome of Puumala hantavirus (PUUV) infection shows extensive variation, ranging from inapparent subclinical infection (70–80%) to severe hemorrhagic fever with renal syndrome (HFRS), with about 0.1% of cases being fatal. Most hospitalized patients experience acute kidney injury (AKI), histologically known as acute hemorrhagic tubulointerstitial nephritis. Why this variation? There is no evidence that there would be more virulent and less virulent variants infecting humans, although this has not been extensively studied. Individuals with the human leukocyte antigen (HLA) alleles B*08 and DRB1*0301 are likely to have a severe form of the PUUV infection, and those with B*27 are likely to have a benign clinical course. Other genetic factors, related to the tumor necrosis factor (TNF) gene and the C4A component of the complement system, may be involved. Various autoimmune phenomena and Epstein-Barr virus infection are associated with PUUV infection, but hantavirus-neutralizing antibodies are not associated with lower disease severity in PUUV HFRS. Wide individual differences occur in ocular and central nervous system (CNS) manifestations and in the long-term consequences of nephropathia epidemica (NE). Numerous biomarkers have been detected, and some are clinically used to assess and predict the severity of PUUV infection. A new addition is the plasma glucose concentration associated with the severity of both capillary leakage, thrombocytopenia, inflammation, and AKI in PUUV infection. Our question, “Why this variation?” remains largely unanswered.

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Haemorrhagic fever with renal syndrome and other hantavirus infections

Lundkvist

Niklasson²

1994

Reviews in Medical Virology

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Anti-endothelial cell antibodies in nephropathia epidemica and other viral diseases

Cited by 20 publications

References 27 publications

Autoimmune-Mediated Vascular Injury Occurs Prior to Sustained Hyperglycemia in a Murine Model of Type I Diabetes Mellitus

Autoimmune-Mediated Vascular Injury Occurs Prior to Sustained Hyperglycemia in a Murine Model of Type I Diabetes Mellitus

Puumala Hantavirus Infections Show Extensive Variation in Clinical Outcome

Haemorrhagic fever with renal syndrome and other hantavirus infections

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