Different patterns of some systemic immunological cell markers in HIV only, and HIV/hepatitis C-infected children.

In three groups of children, aged 4-6 years (i.e., human immunodeficiency virus [HIV]-negative controls, HIV-seropositive, and dually HIV/hepatitis C virus (HCV)-seropositive), two types of immunological investigations in blood cells were performed: (a) numerical assays, consisting of flow cytometric measurement of different lymphocyte sets or subsets, as follows: CD3+, CD19+, CD4+, CD16+/CD56+; (b) functional assays, consisting of interleukin-1 (IL-1) levels as well as natural killer (NK)-cell dependent cytotoxicity, in CD14+, or CD16+/CD56+ sorted cells, respectively. Results revealed, in addition to the classic markers (i.e., lower numbers of CD4+ cells and a decreased CD4+/CD8+ ratio in both infected groups of subjects) other findings, as follows: increased numbers of CD8+ cells in dually infected children, accompanied by a lower CD4+/CD8+ ratio, as compared to HIV-infected alone; diminished numbers of CD16+/CD56+ cells in both groups of infected patients were correlated with a lower NK-cell cytotoxicity rate; a reduced capacity for IL-1 synthesis of sorted macrophages both in HIV-only and in HIV/HCV-seropositive subjects, but significantly more marked in dually infected children. The importance of the present data in the immune monitoring of AIDS disease in a pediatric population is discussed.

Modulation of mouse spleen natural killer (NK) cell activity by beta-interferon, interleukin-1, and prostaglandins.

By using CBA/J mice as a source of effector cells and Yac-1 lymphoma line as "target" cells, the natural killer (NK) cell activity was assayed following both in vivo and in vitro immunomodulation [beta-interferon (IF), interleukin-1 (IL-1), indomethacin (IND), prostaglandin-E2 (PGE)]. Only IF/IND and IL-1/IND mixed in vivo led to a significant augmentation of NK cell activity. If exposed in vitro to IF or to IL-1, control group-derived spleen NK cells exhibited increased cytotoxic activity whereas PGE-exposure only was followed by a lower cytotoxic level as expressed both in % cytotoxicity curves and in lytic units 20%/10(7) effector cells. On the other hand, PGE seemed to activate the "nonspecific suppressor" (NSS) cell subset in its inhibitory effect about NK cells as tested in vitro in several NK/NSS cell mixtures at different ratios. IF, but not IL-1 diminished the NSS-cell-induced suppressive activity. Pre-exposure of NK/NSS cell mixtures to IF followed by PGE exposure, did not prevent PGE-dependent NSS cell activation.