ArticleClinical and experimental immunology2004
Prospective immunological profiling in a case of immune dysregulation, polyendocrinopathy, enteropathy, X-linked syndrome (IPEX).
Article in Clinical and experimental immunology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- IL-7 administration to humans leads to expansion of CD8+ and CD4+ cells but a relative decrease of CD4+ T-regulatory cells.Journal of immunotherapy (Hagerstown, Md. : 1997)Trial
- Single-cell analysis of FOXP3 deficiencies in humans and mice unmasks intrinsic and extrinsic CD4Nature immunology · 2021Observational
- Circulating L-selectin expressing-T cell subsets correlate with the severity of Foxp3 deficiency autoimmune disease.International journal of clinical and experimental pathology · 2016Article
- Primary immune deficiency disorders presenting as autoimmune diseases: IPEX and APECED.Journal of clinical immunology · 2008Review
- Genes mediating environment interactions in type 1 diabetes.The review of diabetic studies : RDS · 2005Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
IPEX syndrome is a genetic autoimmune disease characterized by immune-mediated polyendocrinopathy, enteropathy, and X-linked inheritance. We describe a case of IPEX in which lymphocyte phenotypes were assessed at birth, before initiation of Cyclosporin A therapy, and at frequent intervals to 18 months of age. We performed flow cytometry for lymphocyte subtypes and for activation markers (HLA-DR, CD25, and CD69 or CD71). The ratios of both T to B cells and CD4+ to CD8+ cells were elevated at birth, but CD4+ cells were not activated. HLA-DR+ and CD25+ activated T-cells increased in association with two episodes of clinical deterioration: colitis and the onset of type I diabetes mellitus. These results indicate that measures of activation, particularly HLA-DR+ and CD25+ frequency, correlate well with the development of early active disease and may presage clinical episodes. Continuous maintenance of immunosuppression, once started, appears critical for prevention of permanent tissue damage.
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