ArticleClinical and experimental immunology2006
Maturational alterations of peripheral T cell subsets and cytokine gene expression in 22q11.2 deletion syndrome.
Article in Clinical and experimental immunology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 32 citations in OpenAlex.
- Transgenic expression of microRNA-185 causes a developmental arrest of T cells by targeting multiple genes including Mzb1.The Journal of biological chemistry · 2013Trial
- Trial
- Follicular Helper T Cells and B Cell Maturation in Patients with 22q11.2 Deletion Syndrome and Recurrent Infections.Journal of clinical immunology · 2026Article
- Clinical Practice Guidelines for the Immunological Management of Chromosome 22q11.2 Deletion Syndrome and Other Defects in Thymic Development.Journal of clinical immunology · 2023Review
- Downregulation of miR-185 is a common pathogenic event in 22q11.2 deletion syndrome-related and idiopathic schizophrenia.Metabolic brain disease · 2022Article
- Molecular Insights Into the Causes of Human Thymic Hypoplasia With Animal Models.Frontiers in immunology · 2020Review
- Variable immune deficiency related to deletion size in chromosome 22q11.2 deletion syndrome.American journal of medical genetics. Part A · 2018Review
- A pilot study on immuno-psychiatry in the 22q11.2 deletion syndrome: A role for Th17 cells in psychosis?Brain, behavior, and immunity · 2018Article
- Clinical Phenotype of DiGeorge Syndrome with Negative Genetic Tests: A Case of DiGeorge-Like Syndrome?Case reports in pediatrics · 2015Article
- Functional gene-expression analysis shows involvement of schizophrenia-relevant pathways in patients with 22q11 deletion syndrome.PloS one · 2012Article
- Secondary immunologic consequences in chromosome 22q11.2 deletion syndrome (DiGeorge syndrome/velocardiofacial syndrome).Clinical immunology (Orlando, Fla.) · 2010Article
- Persistent low thymic activity and non-cardiac mortality in children with chromosome 22q11.2 microdeletion and partial DiGeorge syndrome.Clinical and experimental immunology · 2009Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chromosome 22q11.2 deletion syndrome is a common disorder characterized by thymic hypoplasia, conotruncal cardiac defect and hypoparathyroidism. Patients have a risk of infections and autoimmunity associated with T lymphocytopenia. To assess the immunological constitution of patients, the numerical changes and cytokine profile of circulating T cells were analysed by flow cytometry and real-time polymerase chain reaction (PCR). CD3+, CD4+, T cell receptor (TCR)alphabeta+ or CD8alphaalpha+ cell counts were lower, and CD56+ cell counts were higher in patients than in controls during the period from birth to adulthood. The ageing decline of CD3+ or CD4+ cell counts was slower in patients than in controls. The proportion of CD8alphaalpha+ cells increased in controls, and the slope index was larger than in patients. On the other hand, both the number and proportion of Valpha24+ cells increased in patients, and the slope indexes tended to be larger than in controls. The positive correlation of the number of T cells with CD8alphaalpha+ cells was observed only in patients, and that with Valpha24+ cells was seen only in controls. No gene expression levels of interferon (IFN)-gamma, interleukin (IL)-10, transforming growth factor (TGF)-beta, cytotoxic T lymphocyte antigen 4 (CTLA4) or forkhead box p3 (Foxp3) in T cells differed between patients and controls. There was no significant association between the lymphocyte subsets or gene expression levels and clinical phenotype including the types of cardiac disease, hypocalcaemia and frequency of infection. These results indicated that T-lymphocytopenia in 22q11.2 deletion patients became less severe with age under the altered composition of minor subsets. The balanced cytokine profile in the limited T cell pool may represent a T cell homeostasis in thymic deficiency syndrome.
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