[Changes in CD69, CD25 and HLA-DR expressions in peripheral blood T cells in Kawasaki disease].
OBJECTIVE
The study was designed to investigate the changes in CD(69), CD(25) and HLA-DR expressions in peripheral blood T cell in Kawasaki disease (KD).


METHODS
The authors detected CD(69), CD(25) and HLA-DR expressions in peripheral blood T cell by using flow cytometry. The patients who met the diagnostic criteria for KD comprised sixteen boys and fifteen girls (4 - 60 months of age; mean, 26 +/- 18 months). All received intravenous gammaglobulin at a dose of 1 g/(kg.d), for 2 days and oral aspirin at a dose of 30 - 50 mg/(kg.d). In case of persistent fever, a repeated dose of intravenous gammaglobulin or I.V. methylprednisolone at a dose of 20 mg/(kg.d) for three daily doses was attempted. The authors tested blood samples from 17 healthy controls consisting of nine boys and eight girls (3 - 84 months of age; mean, 25 +/- 18 months) and the samples from 31 patients.


RESULTS
The percentage of peripheral blood CD(3)(+) T lymphocyte was (54.4 +/- 9.0)% in acute stage of KD and (65.0 +/- 7.0)% in healthy controls. There was a significant difference between the two groups (P < 0.001). The values of CD(69)(+) [(11.2 +/- 12.6)%, vs. (0.6 +/- 0.4)%], CD(25)(+) [(9.2 +/- 3.5)% vs. (3.9 +/- 1.8)%] and HLA-DR(+) [(8.3 +/- 5.0)% vs. (4.3 +/- 2.3)%] in KD patients were markedly increased compared to those of the healthy controls. After intravenous gammaglobulin treatment, the percentage of CD(3)(+)CD(69)(+) and CD(3)(+)CD(25)(+) significantly decreased [CD(3)(+)CD(69)(+): (14.0 +/- 13.0)% vs. (1.6 +/- 1.2)%, P < 0.05; CD(3)(+)CD(25)(+): (7.8 +/- 4.1)% vs. (2.0 +/- 0.6)%, P < 0.01]. However, the CD(3)(+) T lymphocytes increased [(50.8 +/- 5.0)% vs. (64.9 +/- 5.5)%, P < 0.01]. There was no significant difference in expression of CD(3)(+) T lymphocyte cell activating markers between coronary artery disease group and normal coronary artery group in KD cases (P > 0.05).


CONCLUSIONS
CD(3)(+) T cell activation in the early and middle stages is involved in the mechanism responsible for cardiovascular injury.
Zhang
Yi-ying
YY
Department of Cardiology, Children's Hospital Affiliated to Medical College, Zhejiang University, Hangzhou 310003, China.
Huang
Xian-mei
XM
Kang
Man-li
ML
Gong
Fang-qi
FQ
Qian
Bai-qin
BQ
D015703:Antigens, CD / Q000097:blood*; D000945:Antigens, Differentiation, T-Lymphocyte / Q000097:blood*; D001241:Aspirin / Q000008:administration & dosage / Q000627:therapeutic use; D015415:Biomarkers / Q000097:blood; D002675:Child, Preschool; D004305:Dose-Response Relationship, Drug; D004359:Drug Therapy, Combination; D005260:Female; D005434:Flow Cytometry; D005938:Glucocorticoids / Q000627:therapeutic use; D006684:HLA-DR Antigens / Q000097:blood*; D006801:Humans; D016756:Immunoglobulins, Intravenous / Q000627:therapeutic use; D007155:Immunologic Factors / Q000627:therapeutic use; D007223:Infant; D053645:Interleukin-2 Receptor alpha Subunit / Q000097:blood*; D037181:Lectins, C-Type / Q000097:blood*; D008297:Male; D008775:Methylprednisolone / Q000627:therapeutic use; D009080:Mucocutaneous Lymph Node Syndrome / Q000097:blood / Q000175:diagnosis / Q000188:drug therapy / Q000276:immunology*; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D011379:Prognosis; D013601:T-Lymphocytes / Q000187:drug effects / Q000276:immunology*; D016896:Treatment Outcome; D000099192:CD69 Antigens
D015703:Antigens, CD; D000945:Antigens, Differentiation, T-Lymphocyte; D001241:Aspirin; D015415:Biomarkers; D005938:Glucocorticoids; D006684:HLA-DR Antigens; D016756:Immunoglobulins, Intravenous; D007155:Immunologic Factors; D053645:Interleukin-2 Receptor alpha Subunit; D037181:Lectins, C-Type; D008775:Methylprednisolone; D010975:Platelet Aggregation Inhibitors; D000099192:CD69 Antigens