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Circulation. 2000;102:1114-1119

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(Circulation. 2000;102:1114.)
© 2000 American Heart Association, Inc.


Clinical Investigation and Reports

Evidence for Antigen-Driven T-Cell Response in Unstable Angina

Giuseppina Caligiuri, MD, PhD; Gabrielle Paulsson, PhD; Antonino Nicoletti, PhD; Attilio Maseri, MD; Göran K. Hansson, MD, PhD

From the Center for Molecular Medicine (G.C., G.P., A.N., G.K.H.), Karolinska Institute, Stockholm, Sweden; INSERM U460 (G.C.), Hôpital Bichat, and INSERM U430 (A.N.), Hôpital Broussais, Paris, France; and the Cardiology Institute (A.M.), Catholic University, Rome, Italy.

Correspondence to Dr Giuseppina Caligiuri, INSERM U460, Hôpital Xavier Bichat, 16, rue Henri Huchard, 75018 Paris, France. E-mail caligiu{at}bichat.inserm.fr

Background—Activation of T cells and macrophages has been associated with unstable angina (UA), but whether this reflects specific immune responses remains unclear.

Methods and Results—We analyzed the repertoire and the length of complementarity-determining region 3 of the T-cell receptor (TCR) ß-chain variable (BV) gene segments of activated lymphocytes in 23 patients with UA, 13 patients with chronic stable angina (CSA), and 6 normal control subjects. We also tested the proliferation of systemic T cells in response to autologous coronary plaque proteins, oxidized LDL, and Chlamydia pneumoniae as candidate antigens, in vitro. The activated T cell–TCRBV repertoire was perturbed in 13 (57%) of 23 UA patients versus 3 (23%) of 13 CSA patients (P=0.016) and was restricted to 6 (28%) of 21 expanded TCRBV families; all were significantly higher in UA than in CSA patients. At least one monotypic or oligotypic activated TCRBV population was found in 15 (65%) of 23 UA patients and in 3 (23%) of 13 CSA patients (P<0.001). Finally, T cells from UA patients, but not from CSA patients or normal control subjects, proliferated in response to autologous proteins from coronary culprit lesions and/or to oxidized LDL.

Conclusions—Our findings suggest that the T-cell response observed in UA patients is antigen-driven and directed to antigens contained in the culprit coronary atherosclerotic plaques.


Key Words: angina • ischemia • prognosis • lymphocytes • antigens




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