These cells were formerly known as suppressor T cells. The "classic" T regulatory cells (T-regs) express CD4, CD25 and FOXP3. T regulatory cells (Treg) are distinguished by CD4+, CD25+, GITR+, CTLA-4+. Some of T regs also express the transcription factor Foxp3 (nTreg).
This study from Turkey investigated the long-term outcome for children with asthma to determine the risk factors in predicting persistence of disease. It included 62 children with asthma who were evaluated retrospectively at the end of a 10 year follow-up (mean age at final assessment was 15.9 years).
50% percent of patients outgrew their asthma during the 10 year follow-up period. All the non-atopic patients outgrew their disease during the study period, whereas 67% of atopic patients did not.
Two risk factors were independently related to the persistence of symptoms: bronchial hyperresponsiveness and rhinitis. Atopic children who were in remission demonstrated significantly higher allergen-induced CD4+CD25+ T cells compared to healthy controls.
Atopy, rhinitis and bronchial hyperreactivity are important risk factors for the persistence of asthma in children. Allergen-induced CD4+CD25+ T cells were higher in the atopic children who outgrew their disease, implicating an immunological mechanism of asthma remission in children.
Treg subsets include:
- Natural Tregs (nTreg). nTregs develop in the thymus and constitutively express Foxp3 and CD25. They depend upon IL-2 for their survival.
- Induced Tregs (iTreg). iTregs are induced from naïve CD4 in the periphery. They express Foxp3 only after development by TGF-b.
- T Regulatory 1 (Tr1). Tr1 do not express CD25 or Foxp3. They depend on IL-10 from DCs for development. Tr1 produce high levels of IL-10.
Regulatory T cells - 6 groups have been described (click to enlarge the image).
Reference:
Risk Factors for Persistence of Asthma in Children: 10 Year Follow-up. Aydogan M, Ozen A, Akkoc T, Eifan A, Aktas E, Deniz G, Gocmen I, Bahceciler NN, Barlan I. J Asthma. 2013 Aug 6.
http://www.ncbi.nlm.nih.gov/pubmed/23919566
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