title: Levels and function of regulatory T cells in patients with polymorphic light eruption: relation to photohardening.
abstract: BACKGROUND
  We hypothesized that regulatory T cells (Tregs) are involved in the immunological abnormalities seen in patients with polymorphic light eruption (PLE).
  
  
  OBJECTIVE
  To investigate the number and suppressive function of peripheral Tregs in patients with PLE compared with healthy controls.
  
  
  METHODS
  Blood sampling was done in 30 patients with PLE [seeking or not seeking 311-nm ultraviolet (UV)B photohardening] as well as 19 healthy controls at two time points: TP1, March to June (before phototherapy); and TP2, May to August (after phototherapy). We compared the number of CD4(+) CD25(high) CD127(-) FoxP3(+) Tregs by flow cytometry and their function by assessing FoxP3 mRNA levels and effector T cell/Treg suppression assays.
  
  
  RESULTS
  Tregs isolated from healthy controls significantly suppressed the proliferation of effector T cells at TP1 by 68% (P = 0·0156). In contrast, Tregs from patients with PLE entirely lacked the capacity to suppress effector T-cell proliferation at that time point. The medical photohardening seen in 23 patients with PLE resulted in a significant increase in the median percentage of circulating Tregs [both as a proportion of all lymphocytes; 65 6% increase (P = 0·0049), and as a proportion of CD4(+) T cells; 32.5% increase (P = 0·0049)]. This was accompanied by an increase in the expression of FoxP3 mRNA (P = 0·0083) and relative immunosuppressive function of Tregs (P = 0·083) comparing the two time points in representative subsets of patients with healthy controls tested. Seven patients with PLE not receiving 311-nm UVB also exhibited an increase in the number of Tregs but this was not statistically significant. No significant differences in Treg numbers were observed in healthy subjects between the two time points.
  
  
  CONCLUSIONS
  An impaired Treg function is likely to play a role in PLE pathogenesis. A UV-induced increase in the number of Tregs (either naturally or therapeutically) may be a compensatory mechanism by which the immune system counteracts the susceptibility to PLE.
authors.affiliation: Research Unit for Photodermatology, Department of Dermatology, Medical University of Graz, Auenbrugger Platz 8, A-8036, Graz, Austria.|Center for Medical Research, Medical University of Graz, Auenbrugger Platz 8, A-8036, Graz, Austria.
authors.forename: N
authors.initials: N
authors.lastname: Schweintzger
authors.affiliation: Research Unit for Photodermatology, Department of Dermatology, Medical University of Graz, Auenbrugger Platz 8, A-8036, Graz, Austria.
authors.forename: A
authors.initials: A
authors.lastname: Gruber-Wackernagel
authors.affiliation: Research Unit for Photodermatology, Department of Dermatology, Medical University of Graz, Auenbrugger Platz 8, A-8036, Graz, Austria.|Center for Medical Research, Medical University of Graz, Auenbrugger Platz 8, A-8036, Graz, Austria.
authors.forename: E
authors.initials: E
authors.lastname: Reginato
authors.affiliation: Center for Medical Research, Medical University of Graz, Auenbrugger Platz 8, A-8036, Graz, Austria.
authors.forename: I
authors.initials: I
authors.lastname: Bambach
authors.affiliation: Institute for Medical Informatics, Statistics and Documentation, Medical University of Graz, Auenbrugger Platz 8, A-8036, Graz, Austria.
authors.forename: F
authors.initials: F
authors.lastname: Quehenberger
authors.affiliation: Cellular Photoimmunology Group, Infectious Diseases and Immunology, Sydney Medical School, The Charles Perkins Centre Hub at The University of Sydney, Australia.
authors.forename: S N
authors.initials: SN
authors.lastname: Byrne
authors.affiliation: Research Unit for Photodermatology, Department of Dermatology, Medical University of Graz, Auenbrugger Platz 8, A-8036, Graz, Austria.
authors.forename: P
authors.initials: P
authors.lastname: Wolf
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D049109:Cell Proliferation / Q000502:physiology; D005260:Female; D051858:Forkhead Transcription Factors / Q000378:metabolism; D006801:Humans; D008297:Male; D008875:Middle Aged; D010787:Photosensitivity Disorders / Q000276:immunology* / Q000378:metabolism / Q000532:radiotherapy; D012621:Seasons; D050378:T-Lymphocytes, Regulatory / Q000378:metabolism / Q000502:physiology*; D014467:Ultraviolet Therapy / Q000379:methods*; D015854:Up-Regulation / Q000502:physiology; D055815:Young Adult
chemical_list: C418974:FOXP3 protein, human; D051858:Forkhead Transcription Factors