Abstract
We thank Ammirati et al for their comments on our recent article describing the role of costimulatory receptors OX40 and 4-1BB of the tumor necrosis factor receptor superfamily in CD4+CD28null T cells from acute coronary syndrome (ACS) patients.1 The role of inflammation and immune activation in atherosclerosis has been widely recognized for some time now; however, selective immunomodulatory therapies that enable elimination of proatherogenic while preserving atheroprotective immune cells have yet to make their way into the clinical arsenal. CD4+CD28null T cells are an unusual subset of lymphocytes rarely encountered in healthy individuals but substantially upregulated in patients with chronic inflammatory disorders. These cells lack the costimulatory receptor CD28 that is critical for optimal T-cell activation after antigen recognition. Noteworthy, CD4+CD28null T cells have a unique phenotype that distances them clearly from conventional helper CD4+CD28+ T cells.2 Indeed, CD4+CD28null T cells release high levels of proinflammatory cytokines interferon-γ and tumor necrosis factor-α and express cytotoxic molecules (eg, perforin and granzyme B) in the resting state and after activation. Our work shows that CD4+ …
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