Cytokines from Lymphoid Organs of HIV‐infected Patients: Production and Role in the Immune Disequilibrium of the Disease and in the Development of B Lymphomas

Émilie, Dominique; Ftor, Renato; Llorente, Lurs; Marfaing-Koka, Anne; Devergne, Odile; Jarrousse, B; Wijdenes, John; Galanaud, Pierre

doi:10.1111/j.1600-065x.1994.tb00863.x

Cited by 40 publications

(25 citation statements)

References 123 publications

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“…We confirm our previous observations and those of others which suggest that unstimulated PBMC from HIV þ individuals produce high levels of IL-10 compared with that produced by HIV -individuals [25,28]. However, different investigators have reported variable results for IL-10 secretion following PHA stimulation of PBMC from HIV þ individuals.…”

Section: Discussionsupporting

confidence: 82%

“…The mechanism by which IL-10 induces immunosuppression has been attributed in part to its inhibitory effects on the synthesis of cytokines such as IL-2, IL-12 and interferon-gamma (IFN-g) [17][18][19]47] and inhibiting B7.2 expression on APC [16,48]. Increased expression of IL-10 [23,40,41] and decreased production of IL-12 by monocytes of HIV þ individuals [28,31] may induce immune unresponsiveness by inhibiting the CD28-B7 pathway, as IL-10 and IL-12 mediate their biological effects by regulating the CD28-B7 pathway [16,49]. The inverse correlation of IL-10 production with proliferative responses to anti-CD28 antibodies and the observation that anti-IL-10 antibodies enhance CD28-mediated proliferation suggest that IL-10 exerts immunosuppressive effects by inhibiting the CD28-B7 pathway in HIV infection.…”

Section: Discussionmentioning

confidence: 99%

“…Increased IL-10 production by phytohaemagglutinin (PHA)-stimulated peripheral blood mononuclear cells (PBMC) from HIV þ individuals has been shown in one study to be inversely associated with IL-2 production following stimulation with recall antigens [24]. However, other studies have shown that PHA-stimulated PBMC from HIV þ individuals produced varying levels of IL-10 [25][26][27][28][29][30][31][32][33][34]. We hypothesized that varying levels of IL-10 produced in response to antigen/mitogen may influence immune responsiveness by modulating CD28-mediated proliferative signals.…”

Section: T Cells Infected In Vitro With Hiv and Cd4mentioning

confidence: 99%

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Differential production of IL-10 by T cells and monocytes of HIV-infected individuals: association of IL-10 production with CD28-mediated immune responsiveness

Kumar

Angel

Daftarian³

et al. 1998

Clinical and Experimental Immunology

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SUMMARYImmune unresponsiveness in HIV-1 infection can result from impaired signals delivered by the costimulatory CD28-B7 pathway and the altered production of immunoregulatory cytokines, in particular IL-10, whose production is altered in HIV-1 infection. In this study we investigate IL-10 regulation in T cells and monocytes from HIV þ individuals, and its association with CD28-mediated T cell proliferation. IL-10 production as analysed in T cell-and monocyte-depleted peripheral blood mononuclear cells (PBMC), and by intracellular staining at the single-cell level, reveals a defect in IL-10 production by CD4 þ and CD8 þ T cells, whereas monocytes constitute the major IL-10-producing cell type. To investigate the impact of IL-10 on immune responsiveness, CD28-mediated proliferative responses in HIV þ individuals were correlated with PHA-induced IL-10 production. CD4 þ T cells expressed CD28, yet exhibited markedly reduced CD28-mediated cell proliferation. This CD28-mediated CD4 þ T cell proliferation was found to be inversely associated with the levels of PHAinduced IL-10 production and could be restored, at least in part, by anti-IL-10 antibodies. These results suggest that IL-10 production is differentially regulated in T cells and monocytes of HIV þ individuals, and that IL-10 may have a role in inducing immune unresponsiveness by modulating the CD28-B7 pathway.

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Section: Discussionsupporting

confidence: 82%

Section: Discussionmentioning

confidence: 99%

Section: T Cells Infected In Vitro With Hiv and Cd4mentioning

confidence: 99%

See 1 more Smart Citation

Differential production of IL-10 by T cells and monocytes of HIV-infected individuals: association of IL-10 production with CD28-mediated immune responsiveness

Kumar

Angel

Daftarian³

et al. 1998

Clinical and Experimental Immunology

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“…Inflammatory cytokine secretion by activated immune cells favors virus replication, regulates lymphocyte traffic, and is instrumental to injury of lymphoid tissue (1)(2)(3). Similarly, leukocyte infiltration and abnormal cytokine response are typical features of HIV-1-associated tissue disorders, including tumors, opportunistic infections, and CNS degeneration (4).…”

Section: Hiv-1 Tat Protein Stimulates In Vivo Vascularmentioning

confidence: 99%

HIV-1 Tat Protein Stimulates In Vivo Vascular Permeability and Lymphomononuclear Cell Recruitment

Arese

Ferrandi

Primo

et al. 2001

The Journal of Immunology

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HIV-1 Tat protein released by infected cells is a chemotactic molecule for leukocytes and induces a proinflammatory program in endothelial cells (EC) by activating vascular endothelial growth factor (VEGF) receptors expressed on both cell types. Its potential role in causing vascular permeability and leukocyte recruitment was studied in vivo following its s.c. injection in mice. Tat caused a dose-dependent early (15 min) and late (6 h) wave of permeability that were inhibited by a neutralizing Ab anti-VEGF receptor type 2. Tissue infiltration of lymphomononuclear cells, mainly monocytes (76%), was evident at 6 h and persisted up to 24 h. WEB2170, a platelet activating factor (PAF) receptor antagonist, reduced the early leakage by 70–80%, but only slightly inhibited the late wave and cell recruitment. In vitro, Tat induced a dose-dependent flux of albumin through the EC monolayer that was inhibited by Ab anti-vascular VEGF receptor type 2 and WEB2170, and PAF synthesis in EC that was blocked by the Ab anti-VEGF receptor type 2. Lastly, an anti-monocyte chemotactic peptide-1 (MCP-1) Ab significantly reduced the lymphomononuclear infiltration elicited by Tat. In vitro, Tat induced a dose-dependent production of MCP-1 by EC after a 24-h stimulation. These results highlighted the role of PAF and MCP-1 as secondary mediators in the onset of lymphomononuclear cell recruitment in tissues triggered by Tat.

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“…The changes in soluble mediator networks characterize the early and late events of HIV-1 infection [103,104] and the abnormal increased of circulating inflammatory cytokines [TNF-a, IL-1, IL-8, monocyte chemotactic peptide (MCP) -1] renders EC more adhesive and favors the diapedesis of circulating cells [17]. Furthermore, the presence of HIV in lymphomononuclear cells, the viral proteins Tat, Nef and gp120 and the unbalance of cytokine system alter the expression of adhesion molecules (CD11a/CD18, CD49d/CD29, CD58, CD62L, CD44) on cell membrane and modify the transmigration properties of circulating cells across the vessel walls [28,70,[106][107][108][109][110][111].…”

Section: Regulation Of Leukocytes Diapedesis By Ecmentioning

confidence: 99%

Interactions between endothelial cells and HIV-1

Bussolino

Mitola

Serini

et al. 2001

The International Journal of Biochemistry &Amp; Cell Biology

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Endothelial cells (EC) participate in inflammatory and immune reactions by producing and responding to soluble mediators. Human immunodeficiency virus (HIV)-1 profoundly alters the features of EC. In some anatomical districts, they are infected by the virus and may represent a relevant reservoir. During lymphomononuclear cell diapedesis, EC activate virus replication in crossing cells. Direct or indirect damage of EC is particularly relevant in central nervous system, where blood-brain barrier perturbation is pivotal in neuronal degeneration. The observed alterations of EC adhesive properties contribute in altered leukocyte traffic from blood to lymphoid organs and tissues and play a role in the onset of immune surveillance alteration. These alterations of EC functions are relevant for the general vasculopathy, which marks the acquired immunodeficiency syndrome, and in particular are instrumental in the pathogenesis of Kaposi's sarcoma. Here we discuss the biological and molecular activation of EC in HIV-1 infection that represents the basis to understand the pathogenesis of HIV-1 associated vascular diseases.

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Cytokines from Lymphoid Organs of HIV‐infected Patients: Production and Role in the Immune Disequilibrium of the Disease and in the Development of B Lymphomas

Cited by 40 publications

References 123 publications

Differential production of IL-10 by T cells and monocytes of HIV-infected individuals: association of IL-10 production with CD28-mediated immune responsiveness

Differential production of IL-10 by T cells and monocytes of HIV-infected individuals: association of IL-10 production with CD28-mediated immune responsiveness

HIV-1 Tat Protein Stimulates In Vivo Vascular Permeability and Lymphomononuclear Cell Recruitment

Interactions between endothelial cells and HIV-1

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