title: [Decrease of FOXP3 mRNA in CD4+ T cells in latent autoimmune diabetes in adult].
abstract: OBJECTIVE
  To study the percentage of peripheral blood CD4(+)CD25(+) T cells and the expression of FOXP3 mRNA in the patients with latent autoimmune diabetes in adult (LADA).
  
  
  METHODS
  Fresh peripheral blood samples were obtained from 60 patients with LADA, 30 patients with type 2 diabetes and 30 age- and sex-matched matched healthy nondiabetic control subjects without diabetic family history. Two-color staining (anti-CD4, anti-CD25, anti-CD3, and anti-CD8) flow cytometric analysis was employed to measure the CD4(+)CD25(+) T cells. The CD4 positive human cells were isolated with immunomagnetic beads, and then real time-PCR was used to test the expression of FOXP3 mRNA in the CD4(+) T cells.
  
  
  RESULTS
  In the LADA group, the percentage of CD4(+)CD25(+) T cells was 4.1 +/- 1.9, significantly higher than that of the normal control group (2.8 +/- 1.5, P < 0.01), the ratio of CD4(+)CD25(+) to the CD4(+) T cells was 11.9 +/- 5.0, significantly higher than that of the normal control group (8.2 +/- 3.7, P < 0.01), the percentage CD8(+) T cells was 24.6 +/- 6.8, significantly higher than that of the normal control group (19.4 +/- 7.1, P < 0.01) and the CD4(+)/CD8(+) ratio was 1.5 +/- 0.5, significantly lower (1.9 +/- 0.6, P < 0.01). The expression of FOXP3 mRNA in CD4(+) T cells of the LADA group was 0.52 time that of the control group (P < 0.01). The CD4(+)/CD8(+) ratio of LADA group was significantly lower that of the type 2 diabetes group (1.8 +/- 0.8, P < 0.05), however, the other results were not significantly different between these 2 groups. The percentage of was positively correlated with the titer of glutamic acid decarboxylase antibody (GADA) (r = 0.292, P < 0.05).
  
  
  CONCLUSIONS
  Though the percentage of CD4(+)CD25(+) T cells and the level of CD25 expression in CD4(+) T cells are elevated, the expression of FOXP3 mRNA in CD4(+) T cells is lower. in the patients with LADA. The regulatory T cells may have defective suppressor function in patients with LADA.
authors.affiliation: Institute of Metabolism and Endocrinology, Second Xiangya Hospital, Diabetes Center of Central South University, Changsha 410011, China.
authors.forename: Zhi-fang
authors.initials: ZF
authors.lastname: Yang
authors.forename: Zhi-guang
authors.initials: ZG
authors.lastname: Zhou
authors.forename: Wei-li
authors.initials: WL
authors.lastname: Tang
authors.forename: Gan
authors.initials: G
authors.lastname: Huang
authors.forename: Jian
authors.initials: J
authors.lastname: Peng
authors.forename: Xia
authors.initials: X
authors.lastname: Li
authors.forename: Ling
authors.initials: L
authors.lastname: He
mesh_terms: D000328:Adult; D000368:Aged; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology* / Q000378:metabolism; D016022:Case-Control Studies; D003922:Diabetes Mellitus, Type 1 / Q000235:genetics / Q000276:immunology*; D015536:Down-Regulation / Q000235:genetics; D005260:Female; D005434:Flow Cytometry; D051858:Forkhead Transcription Factors / Q000235:genetics*; D006801:Humans; D053645:Interleukin-2 Receptor alpha Subunit / Q000276:immunology; D008297:Male; D008875:Middle Aged; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism*; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: C418974:FOXP3 protein, human; D051858:Forkhead Transcription Factors; D053645:Interleukin-2 Receptor alpha Subunit; D012333:RNA, Messenger