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PMID: 17349011 Published · ppublish English Journal Article

The levels of CD4+CD25+ regulatory T cells in paediatric patients with allergic rhinitis and bronchial asthma.

Clinical and experimental immunology ·Vol. 148 ·No. 1 ·2007-04-00 ·Pages 53-63

Lee JH, Yu HH, Wang LC, Yang YH, Lin YT, Chiang BL

Abstract

Our purpose was to determine whether numbers of CD4(+)CD25(+) T [T regulatory (T(reg))] cells and mRNA expression of functional molecules of T(reg) are related to airway allergy and disease severity in 51 paediatric patients with allergic rhinitis or bronchial asthma and 47 healthy controls. Surface markers were evaluated with flow cytometry, and mRNA was determined with real-time polymerase chain reaction. Children with allergic disease had fewer CD4(+)CD25(+) T cells (8 x 49% +/- 2 x 41% versus 9 x 58% +/- 2 x 43%, P<0 x 05) and CD4(+)CD25(hi) T cells (1 x 32% +/- 0 x 68% versus 1 x 70% +/- 0 x 68%, P<0 x 01) than control subjects. Numbers of CD4(+)CD25(+) and CD4(+)CD25(hi) T lymphocytes were higher in children with persistent allergic rhinitis and/or moderate-severe bronchial asthma than in those with respective milder disease. The number of T(reg) cells was correlated positively with total immunoglobulin E level. The mRNA expression of forkhead box P3 (FoxP3) was increased in moderate-severe versus mild asthma (2 x 93 +/- 0 x 38 versus 1 x 60 +/- 0 x 31, P< 0 x 01). Patients with moderate-severe bronchial asthma also had increased mRNA expression of interleukin (IL)-10 compared with patients with mild asthma (15 x 24 +/- 4 x 07 versus 3 x 77 +/- 2 x 18, P<0 x 01). The suppressive function of T(reg) cells from patients with more severe asthma was competent in vitro. On average, decreased numbers of T(reg) cells in children with allergic airway disease might represent a defect of the T(reg) population. With increased expression of FoxP3 and IL-10 in T(reg) from patients with relatively severe allergic disease, adaptive and functional T(reg) might be generated in response to aggravated atopy and disease severity.

MeSH Terms
Antigens, CD/biosynthesis,genetics Antigens, Differentiation/biosynthesis,genetics Asthma/immunology CTLA-4 Antigen Cell Proliferation Cells, Cultured Child Child, Preschool Female Forkhead Transcription Factors/biosynthesis,genetics Gene Expression Glucocorticoid-Induced TNFR-Related Protein Humans Immune Tolerance Immunoglobulin E/blood Interleukin-10/biosynthesis,genetics Interleukin-2 Receptor alpha Subunit/blood Lymphocyte Count Male Polymerase Chain Reaction/methods RNA, Messenger/genetics Receptors, Nerve Growth Factor/biosynthesis,genetics Receptors, Tumor Necrosis Factor/biosynthesis,genetics Rhinitis/immunology Severity of Illness Index T-Lymphocytes, Regulatory/immunology Transforming Growth Factor beta/biosynthesis,genetics
Chemicals
Antigens, CD Antigens, Differentiation CTLA-4 Antigen CTLA4 protein, human FOXP3 protein, human Forkhead Transcription Factors Glucocorticoid-Induced TNFR-Related Protein Interleukin-2 Receptor alpha Subunit RNA, Messenger Receptors, Nerve Growth Factor Receptors, Tumor Necrosis Factor TNFRSF18 protein, human Transforming Growth Factor beta Interleukin-10 Immunoglobulin E
Authors & Affiliations
6 authors, click to expand affiliations / ORCID
Lee J-H
Department of Pediatrics, National Taiwan University Hospital, Taipei, Taiwan, China.
Yu H-H
Wang L-C
Yang Y-H
Lin Y-T
Chiang B-L
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Article Info
Journal
Clinical and experimental immunology
Abbr.
Clin Exp Immunol
ISSN
0009-9104
Published
2007-04-00
Pages
53-63
Language
English
Region
England
NLM ID
0057202
PMCID
PMC1868849
Subset
IM
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