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. 2004 Jun 8;109(22):2744-8.
doi: 10.1161/01.CIR.0000131450.66017.B3. Epub 2004 May 24.

CD4+CD28- T lymphocytes contribute to early atherosclerotic damage in rheumatoid arthritis patients

Roberto Gerli  1 , Giuseppe Schillaci, Andrea Giordano, Elena Bartoloni Bocci, Onelia Bistoni, Gaetano Vaudo, Simona Marchesi, Matteo Pirro, Federica Ragni, Yehuda Shoenfeld, Elmo Mannarino
Affiliations

CD4+CD28- T lymphocytes contribute to early atherosclerotic damage in rheumatoid arthritis patients

Roberto Gerli et al. Circulation. .

Abstract

Background: Peripheral blood expansion of an unusual CD4+ T-cell subset lacking surface CD28 has been suggested to predispose rheumatoid arthritis (RA) patients to develop more aggressive disease. However, the potential association between CD4+CD28null T cells and early atherosclerotic changes in RA has never been investigated.

Methods and results: The number of circulating CD4+CD28null cells was evaluated in 87 RA and 33 control subjects who also underwent evaluation of carotid artery intima-media thickness (IMT) and endothelial function via flow-mediated vasodilation (FMV). Patients had higher IMT and lower FMV compared with control subjects. The frequency of CD4+CD28null cells was significantly higher in patients than in control subjects. Twenty patients with persistent expansion of circulating CD4+CD28null cells had more marked increase of carotid artery IMT and stronger decrease of brachial artery FMV. Blockade of tumor necrosis factor-alpha led to a partial reappearance of the CD28 molecule on the CD4+ cell surface.

Conclusions: Circulating CD4+CD28(null) lymphocytes are increased in RA. Patients with persistent CD4+CD28null cell expansion show preclinical atherosclerotic changes, including arterial endothelial dysfunction and carotid artery wall thickening, more significantly than patients without expansion. These findings suggest a contribution of this cell subset in atheroma development in RA. Moreover, the demonstration that tumor necrosis factor-alpha blockade is able to reverse, at least in part, the CD28 deficiency on the CD4+ cell surface may be of interest for possible innovative therapeutic strategies in cardiovascular diseases.

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