Cited by 225T-cell and B-cell ImmunologyBlood disorders and treatmentsHematopoietic Stem Cell Transplantation

Deficient CD4+ CD25+ FOXP3+ T regulatory cells in acquired aplastic anemia

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Solomou, Elena E., Rezvani, Katayoun, Mielke, Stephan, Malide, Daniela, Keyvanfar, Keyvan, Visconte, Valeria, Kajigaya, Sachiko, Barrett, A. John +1 more·2007·Blood

Abstract

Regulatory T cells are believed to control the development and progression of autoimmunity by suppressing autoreactive T cells. Decreased numbers of CD4(+)CD25(+) FOXP3(+) T cells (Tregs) are associated with impaired immune homeostasis and development of autoimmune diseases. The transcription factors FOXP3 and NFAT1 have key roles in regulatory T-cell development and function. We show that Tregs are decreased at presentation in almost all patients with aplastic anemia; FOXP3 protein and mRNA levels also are significantly lower in patients with aplastic anemia and NFAT1 protein levels are decreased or absent. Transfection of FOXP3-deficient CD4(+)CD25(+) T cells from patients with a plasmid encoding wild-type NFAT1 resulted in increased FOXP3 expression in these cells. By NFAT1 knockdown in CD4(+)CD25(+) T cells, FOXP3 expression was decreased when NFAT1 expression was decreased. Our findings indicate that decreased NFAT1 could explain low FOXP3 expression and diminished Treg frequency in aplastic anemia. Treg defects are now implicated in autoimmune marrow failure.

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Crossref · 10.1182/blood-2007-01-066258

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  • A type 1 T-helper (Th1) cell-skewed response of the adaptive immune system is a major effector of damage and the major source of IFN-g, accompanied by a reduction in regulatory T cells (Tregs) in the marrow.

    “Another major effector of damage is a type 1 T-helper (Th1) cell-skewed response of the adaptive immune system, which was also identified as the major source of IFN-g, accompanied by a reduction in regulatory T cells (Tregs) in the marrow.60”

    From Inflammatory bone marrow microenvironment (2019) · cites this paper as [60]

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Authors
Solomou, E. E., Rezvani, K., Mielke, S., Malide, D., Keyvanfar, K., Visconte, V., Kajigaya, S., Barrett, A. J., & Young, N. S.
Affiliations
  • Hematology Branch and
  • National Institutes of Health (US)
Venue
Blood
Published
2007-09-01
Volume
110
Issue
5
Pages
1603-1606
ISSN
  • 0006-4971 (ISSN-L)
  • 1528-0020
OpenAlex
W2066935327
Cited by
225
References
24
Citations by year
2026: 11 · 2025: 8 · 2024: 10 · 2023: 11 · 2022: 7 · 2021: 11 · 2020: 21 · 2019: 10 · 2018: 18 · 2017: 19 · 2016: 9 · 2015: 11 · 2014: 11 · 2013: 10 · 2012: 11
FWCI
4.59
Type
journal article
Language
en
Open access
Locations
  • Blood (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Institutes of Health
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Blood disorders and treatments
  • Health Sciences › Medicine › Hematology › Hematopoietic Stem Cell Transplantation
Keywords
regulatory T cells, CD4+CD25+ T cells, Foxp3, NFAT1, acquired aplastic anemia, Treg deficiency, immune homeostasis, transcription factors, Treg reprogramming
MeSH terms
Adolescent, Adult, Anemia, Aplastic, Autoimmune Diseases, Cells, Cultured, Female, Gene Expression Regulation, Humans, Male, Middle Aged, Transfection, Autoimmunity, T-Lymphocytes, Regulatory, NFATC Transcription Factors, Forkhead Transcription Factors

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