A black tongue in a young woman

Guinovart, R.M.; Carrascosa, J.M.; Bielsa, Isabel; Rodriguez, Carmen; Ferrándiz, Carlos

doi:10.1111/j.1365-2230.2010.03946.x

Cited by 3 publications

(3 citation statements)

References 4 publications

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“…Two of them were also IgG negative suggesting that CMV primary infection were involved as a triggering or precipitating factor. This complements a recent case report describing a young female developing AAD shortly after undergoing verified CMV infectious mononucleosis [ 19 ]. Another patient initially only positive for IgG became IgM positive for a period of 2 years, suggesting reactivating or secondary CMV infection.…”

Section: Discussionsupporting

confidence: 85%

“…In genetically predisposed individuals, primary CMV infections have been described as triggers of autoimmune disorders, such as vasculitides and scleroderma, which developed concomitantly with or immediately after active CMV infection in previously healthy, immunocompetent subjects [ 16 – 18 ]. Multiple case reports also describe primary, reactivating or persistent CMV infections as possible triggers of autoimmune endocrine diseases such as type 1 diabetes (T1D), Graves’ disease and AAD [ 19 – 22 ]. Importantly, CMV is known to infect and cause cytopathic damage to the adrenal cortex, and may directly cause adrenal insufficiency in infants and in immunodeficient individuals [ 23 – 26 ].…”

Section: Introductionmentioning

confidence: 99%

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Analysis of cellular and humoral immune responses against cytomegalovirus in patients with autoimmune Addison’s disease

et al. 2016

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BackgroundAutoimmune Addison’s disease (AAD) is caused by multiple genetic and environmental factors. Variants of genes encoding immunologically important proteins such as the HLA molecules are strongly associated with AAD, but any environmental risk factors have yet to be defined. We hypothesized that primary or reactivating infections with cytomegalovirus (CMV) could represent an environmental risk factor in AAD, and that CMV specific CD8+ T cell responses may be dysregulated, possibly leading to a suboptimal control of CMV. In particular, the objective was to assess the HLA-B8 restricted CD8+ T cell response to CMV since this HLA class I variant is a genetic risk factor for AAD.MethodsTo examine the CD8+ T cell response in detail, we analyzed the HLA-A2 and HLA-B8 restricted responses in AAD patients and healthy controls seropositive for CMV antibodies using HLA multimer technology, IFN-γ ELISpot and a CD107a based degranulation assay.ResultsNo differences between patients and controls were found in functions or frequencies of CMV-specific T cells, regardless if the analyses were performed ex vivo or after in vitro stimulation and expansion. However, individual patients showed signs of reactivating CMV infection correlating with poor CD8+ T cell responses to the virus, and a concomitant upregulation of interferon regulated genes in peripheral blood cells. Several recently diagnosed AAD patients also showed serological signs of ongoing primary CMV infection.ConclusionsCMV infection does not appear to be a major environmental risk factor in AAD, but may represent a precipitating factor in individual patients.Electronic supplementary materialThe online version of this article (doi:10.1186/s12967-016-0822-z) contains supplementary material, which is available to authorized users.

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Section: Discussionsupporting

confidence: 85%

Section: Introductionmentioning

confidence: 99%

Analysis of cellular and humoral immune responses against cytomegalovirus in patients with autoimmune Addison’s disease

et al. 2016

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“…Some case reports have described the development of adrenocortical insufficiency in connection with herpesvirus infections , and among these, one reported extensive necrosis in the adrenal cortex caused by herpes simplex virus . Having previously demonstrated the expression of TLR‐3 in H295R cells, which was also reported recently in the adrenal gland of a patient with co‐existing Cushing syndrome and AAD , we tested the ability of poly (I : C), a TLR‐3 stimulant able to mimic viral infections , to exert cytotoxicity on H295R cells.…”

Section: Discussionmentioning

confidence: 94%