CD8(+) T cells with high TGF-β1 expression cause lymph node fibrosis following HIV infection

Lymph node (LN) fibrosis resulting in cluster of differentiation (CD) 4(+) T cell reduction following human immunodeficiency virus (HIV) infection is an important step in the pathogenesis of acquired immunodeficiency syndrome. The mechanisms mediating LN fibrosis following HIV infection have not been completely elucidated. In order to investigate the mechanism of LN fibrosis, the expression of transforming growth factor (TGF)-β1 was determined in the LNs of HIV-infected individuals by immunohistochemistry and fluorescence-based flow cytometry. The effect of stimulated CD8+ T cells on collagen secretion by fibroblasts was detected using immunofluorescence staining and western blot analysis. The results demonstrated that the LNs of HIV-infected individuals exhibited a significantly increased proportion of CD8(+) T cells with high TGF-β1 expression. These CD8(+) T cells demonstrated increased CD38 and programmed cell death protein 1 expression and decreased CD127 expression compared with the controls. CD8(+) T cells from the LNs of non-HIV infected individuals expressed a high TGF-β1 level following stimulation with phorbol-12-myristate 13-acetate. These CD8(+)T cells subsequently induced the secretion of a large amount of type I collagen in human lymphatic fibroblasts. The results of the present study indicated that CD8(+) T cells with high TGF-β1 expression served an important role in LN fibrosis following HIV infection.