Immune system activation follows inflammation in unstable angina: Pathogenetic implications

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Objectives. The aim of this study was to assess the relations between inflammation, specific immune response and clinical course in unstable angina (UA). Background. Several studies suggest that either inflammation and/or T-cell activation might have a pathogenetic role in UA, but neither their potential reciprocal connection nor their relation to the clinical course is known. Methods. Serum levels of C- reactive protein (CRP) (inflammation), IgG, IgA, IgM, C3, C4 (humoral immunity), IL-2 and the percentage of CD4+, CD8+ and CD3+/DR+ T-cells (cell-mediated immunity) were measured in 35 patients with UA and 35 patients with chronic stable angina (CSA) during a period of 6 months. Results. The CRP levels and the main specific immune markers (CD4+ and CD3+/DR+ cells, IL-2 and IgM) were higher in unstable than in stable angina. In UA, the serum levels of IgM and IL-2 and the percentage of double positive CD3+/DR+ significantly increased at 7 to 15 days, and returned to baseline at 6 months. The increment of circulating activated T cells (CD3+/DR+) in UA was inversely related to the admission levels of CRP (r = -0.63, p = 0.003) and associated with a better outcome. Conclusions. Our data suggest that the inflammatory component systemically detectable in UA may be antigen-related and that the magnitude of the immune response correlates with the clinical outcome of instability.




Caligiuri, G., Liuzzo, G., Biasucci, L. M., & Maseri, A. (1998). Immune system activation follows inflammation in unstable angina: Pathogenetic implications. Journal of the American College of Cardiology, 32(5), 1295–1304.

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