title: Acute T-cell activation is detectable in unstable angina.
abstract: BACKGROUND
  Recent studies suggest a role for inflammation in the pathophysiology of unstable angina. This study was designed to investigate whether circulating lymphocytes are involved in the inflammatory reaction associated with the episodes of unstable angina.
  
  
  RESULTS
  Twenty-nine patients with proven unstable angina, 36 with stable angina, and 30 healthy subjects were studied. Both early and short-lived (interleukin-2 receptor [IL-2R], alpha-chain CD25, and transferrin receptor CD71) and late antigen (HLA-DR) expression were investigated by flow cytometric analysis. Soluble IL-2R (sIL-2R) was also measured in plasma by ELISA. Lymphocyte activation was studied at day 1 of hospital admission and after 7, 15, 30, 60, and 90 days. In patients with unstable angina, the number of HLA-DR+ CD3 lymphocytes and levels of sIL-2R were higher (P < .001) than in patients with stable angina and control subjects. Both CD4+ and CD8+ lymphocytes expressed HLA-DR antigens. No differences were found among the different groups of subjects in regard to the expression of CD25 and CD71. Lymphocyte activation was more marked in patients with urgent revascularization. No relationships were found between the number of HLA-DR+ lymphocytes and either the severity of coronary angiographic lesions or the number of ischemic episodes. Observations over time showed a gradual decrease in the number of HLA-DR+ lymphocytes and sIL-2R levels from weeks 3 through 8 to 12.
  
  
  CONCLUSIONS
  The present results indicate that (1) CD4+ and CD8+ circulating lymphocytes are activated in patients with unstable angina, and their activation state lasts 6 to 8 weeks; and (2) activation of lymphocytes is not a consequence of myocardial ischemia. These results support the immune system-mediated inflammatory nature of unstable angina.
authors.affiliation: Clinica Medica Generale e Cardiologia, Florence, Italy.
authors.forename: G G
authors.initials: GG
authors.lastname: Neri Serneri
authors.forename: D
authors.initials: D
authors.lastname: Prisco
authors.forename: F
authors.initials: F
authors.lastname: Martini
authors.forename: A M
authors.initials: AM
authors.lastname: Gori
authors.forename: T
authors.initials: T
authors.lastname: Brunelli
authors.forename: L
authors.initials: L
authors.lastname: Poggesi
authors.forename: C
authors.initials: C
authors.lastname: Rostagno
authors.forename: G F
authors.initials: GF
authors.lastname: Gensini
authors.forename: R
authors.initials: R
authors.lastname: Abbate
mesh_terms: D000368:Aged; D000787:Angina Pectoris / Q000276:immunology; D000789:Angina, Unstable / Q000276:immunology*; D015703:Antigens, CD / Q000032:analysis; D000945:Antigens, Differentiation, T-Lymphocyte / Q000032:analysis; D001161:Arteriosclerosis / Q000150:complications / Q000000981:diagnostic imaging / Q000276:immunology; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology; D017023:Coronary Angiography; D005260:Female; D006684:HLA-DR Antigens / Q000032:analysis; D006801:Humans; D007249:Inflammation; D008213:Lymphocyte Activation; D008297:Male; D008875:Middle Aged; D016176:T-Lymphocyte Subsets / Q000276:immunology*
chemical_list: D015703:Antigens, CD; D000945:Antigens, Differentiation, T-Lymphocyte; D006684:HLA-DR Antigens