Single cell analysis of IL-4 and IFN-gamma production by T cells from HIV-infected individuals: decreased IFN-gamma in the presence of preserved IL-4 production.
J Immunol
; 157(6): 2712-8, 1996 Sep 15.
Article
em En
| MEDLINE
| ID: mdl-8805678
ABSTRACT
The specific in vitro disturbance of capacities ascribed to Th1 cells in HIV-infected individuals suggests a switch from Th1 to Th2 lymphokine secretion. Indeed, when T cell clones are generated from HIV-infected individuals compared with controls, an increased percentage of Th0 clones is present upon HIV infection. We studied cytokine production in the supernatant of in vitro activated PBMC from a large group of HIV-infected patients at various stages of infection. IL-2, IFN-gamma, IL-4, IL-5, and IL-10 production all were decreased significantly, which does not support a switch to Th2 lymphokine secretion and is possibly due to the generalized impaired response of T cells from HIV-infected individuals to activation signals in vitro. Therefore, we investigated the capacity of single cells to produce a certain cytokine. Intracellular staining of IL-4- and IFN-gamma-producing cells revealed that T cells from HIV-infected individuals contained decreased numbers of IFN-gamma-producing cells, in the presence of normal percentages of cells with the capacity to produce IL-4. This resulted in significantly decreased IFN-gamma/IL-4 ratios in both CD4+ and CD8+ T cells. Thus, in agreement with previous findings in T cell clones, we conclude, from cytokine production upon stimulation of T cells in vitro, that there is a change in the cytokine balance to the Th2 side in HIV infection due to decreased Th1 and preserved Th2 cytokine production.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Linfócitos T
/
Infecções por HIV
/
Interleucina-4
/
Interferon gama
Tipo de estudo:
Clinical_trials
/
Etiology_studies
/
Incidence_studies
/
Observational_studies
/
Risk_factors_studies
Limite:
Humans
/
Male
Idioma:
En
Revista:
J Immunol
Ano de publicação:
1996
Tipo de documento:
Article