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CD27− B-cells expressing intracellular IgG have previously also been found to be expanded in patients suffering with systemic lupus erythematosus (SLE) [42].
CD16-positive monocytes were soon demonstrated to be expanded in patients with acute and chronic inflammatory diseases including atherosclerosis and these cells responded with a stronger activation upon inflammatory stimuli [20,21,43].
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Thus, the CD16+ Mo subset is expanded in patients with AIDS, but expansion of this Mo subset is not significantly different between HAD subjects and those with no NCI in this study cohort.
The CD14++CD16+ subset are expanded in patients with rheumatoid arthritis [ 39].
Thus, the CD27-negative subset, which is expanded in patients, contains precursors of IFN- γ-producing effector CD8+ T cells.
Thus, while this subset of effector cells was expanded in patients with cancer, a higher proportion of the cells were in early apoptosis in patients than in NC.
Phenotypic and functional data demonstrate that in SLE patients, CD4+CD25low/-GITR+ cells are fully active Treg cells, possibly representing peripheral Treg (pTreg) that are expanded in patients with inactive disease.
They are pathogenic in the collagen-induced arthritis model [ 47] and mouse models of colitis [ 48], and IL-17secreting γδ T cells are expanded in patients with AS[ 49].
We have previously demonstrated that CD16-expressing mature monocytes – a subpopulation of cells that, while in the circulation, has acquired features in common with proinflammatory tissue macrophages – are expanded in patients with active disease.
Thus, although this subset of effector cells was expanded in patients relative to NC, the near absence of ζ expression in effector T cells suggested that their signalling via TcR was compromised.
8 The domain of loricrin expression was expanded in patient hyperkeratotic skin, with nucleolar expression of loricrin as previously reported with insertions (Fig. 2b).
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