Characterization of the effect of histone deacetylation inhibitors on CD8 T cells in the context of aging.

Background: Posttranslational protein modifications regulate essential cellular processes, including the immune cell activation. Despite known age-related alterations of the phenotype, composition and cytokine profiles of immune cells, the role of acetylation in the aging process of the immune system was not broadly investigated. Therefore, in the current study the effect of acetylation on the protein expression profiles and function of CD8 T cells from donors of distinct age was analyzed using histone deacetylase inhibitors (HDACi).

Transcriptional Analysis of Total CD8 T Cells and CD8CD45RA Memory T Cells From Young and Old Healthy Blood Donors.

Memory CD8 T cells accumulate with aging, while the naïve T cell compartment decreases, leading to an increased susceptibility to infections and a decreased vaccine efficiency. To get deeper insights into the underlying mechanisms, this study aims to determine the age-dependent expression profile of total versus memory CD8 T cells from young and old donors. Total CD8 and CD8CD45RA memory T cells isolated from young (<30 years) and old (>60 years) donors were stimulated with anti-CD3 and anti-CD28 antibodies for 48h before analyzing the cytokine secretion and activation markers by flow cytometry and changes in the expression profiles using RNA sequencing.

[Natural killer cell immunodeficiency and herpesvirus infection in tuberculosis].

An inverse correlation was shown between the activity of natural killer cells (NKC) and the activated infection to herpes simplex virus (HSV)-1 and HSV-2. There was a significant reduction in CD56+ cells in patients who had a history of a concomitance of pulmonary tuberculosis and HSV-2 infection. In patients with tuberculosis, the decreased activity of NKC may activate HSV-1 infection, with its further involvement as an independent factor in the development of meningoencephalitis.

[The role of herpes simplex of type 1 infection in the development of tuberculous meningoencephalitis].

Cases of tuberculous meningoencephalitis in Armenia and a role of the activation of human herpes virus-1 (HHV-1) infection have been investigated. HHV-1 can be an independent factor in the development of meningoencephalitis and a cofactor that produces cellular immunodeficiency in patients with atypical tuberculous meningoencephalitis.