Cytokines in HIV infection

Émilie, Dominique; Fior, R; Jarrousse, B; Marfaing-Koka, Anne; Merrien, Dominique; Devergne, Odile; Crevon, Marie‐Claude; Maillot, M C; Galanaud, Pierre

doi:10.1016/0192-0561(94)90026-4

Cited by 29 publications

(19 citation statements)

References 26 publications

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“…41,59 TNF-␣, which is elevated in HIV infection, activates NF-B and has been shown to promote the growth of KS lesions. 26,60 In confirmation of NF-B inhibition experiments, our data indicate that treatment of KS cells with ritonavir blocked the TNF-␣-induced degradation of IB␣.…”

Section: Discussionsupporting

confidence: 66%

Antitumorigenic effects of HIV protease inhibitor ritonavir: inhibition of Kaposi sarcoma

Pati

Pelser²,

Dufraine³

et al. 2002

Blood

132

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Treatment of patients with human immunodeficiency virus (HIV) protease inhibitors such as ritonavir can result in increases in CD4 ؉ T-cell counts that are independent of a reduction in HIV-1 viral load. This lack of correlation between the 2 has led to the identification of additional effects of ritonavir that potentially alter HIV disease pathogenesis. Our previous studies indicated that ritonavir directly affects immune cell activation, proliferation, and susceptibility to apoptosis. We show here that ritonavir inhibited the activation and proliferation of primary endothelial cells and decreased the produc-

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Section: Discussionsupporting

confidence: 66%

Antitumorigenic effects of HIV protease inhibitor ritonavir: inhibition of Kaposi sarcoma

Pati

Pelser²,

Dufraine³

et al. 2002

Blood

132

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“…18 IL-1 and other cytokines are elevated in circulation during the initial, acute phase of HIV-1 infection and likely play a role in the development of clinical manifestation of AIDS. 19 Circulating IL-1␤ induces another cytokine, TGF-␤1, in astrocytes at the blood-brain barrier (BBB). 18 TGF-␤1 is a potent attractant for monocytes/macrophages 20 and may recruit HIV-1-infected macrophages to enter brain parenchyma.…”

Section: Two Examples Of Upregulation Of Il-1 and Tnf␣ Expression: Aimentioning

confidence: 99%

Cytokine signals propagate through the brain

et al. 2000

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Interleukin-1 (IL-1) and tumor necrosis factor alpha (TNF␣) are proinflammatory cytokines that are constitutively expressed in healthy, adult brain where they mediate normal neural functions such as sleep. They are neuromodulators expressed by and acting on neurons and glia. IL-1 and TNF␣ expression is upregulated in several important diseases/disorders. Upregulation of IL-1 and/or TNF␣ expression, elicited centrally or systemically, propagates through brain parenchyma following specific spatio-temporal patterns. We propose that cytokine signals propagate along neuronal projections and extracellular diffusion pathways by molecular cascades that need to be further elucidated. This elucidation is a prerequisite for better understanding of reciprocal interactions between nervous, endocrine and immune systems. Molecular Psychiatry (2000) 5, 604-615.

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“…Reduced IL-2 formation in HIV-infected patients is well known [23,31,37] and appears to be the cause of decreased lymphocyte proliferation and generation of cytotoxic T lymphocytes [38]. Whether this phenomenon, however, represents a crucial step in the pathogenesis of HIV disease is currently under discussion [39].…”

Section: Discussionmentioning

confidence: 99%

“…In normal volunteers, 9 { 2 pg of IL-4/mL of amounts of proinflammatory cytokines, such as TNF-a [31] blood was released after 48 h in response to SEB. IL-4 amounts and IFN-g [31,32]. These proinflammatory mediators have further increased to 41 { 18 pg/mL of blood when the incubabeen shown to represent endogenous stimuli promoting HIV tion time was extended to 72 h (figure 3B).…”

Section: Study Design and Laboratory Measurementsmentioning

confidence: 99%

Filgrastim Restores Interleukin‐2 Production in Blood from Patients with Advanced Human Immunodeficiency Virus Infection

Hartung

Pitrak²,

Foote³

et al. 1998

J INFECT DIS

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and Albrecht WendelFilgrastim induces lymphocytosis, including all T cell subsets, and increased ex vivo interleukin (IL)-2 release as well as lymphocyte proliferation. Since Filgrastim is increasingly used in patients with human immunodeficiency virus (HIV) infection, the effect of Filgrastim on ex vivo cytokine production was determined. Whole blood from 8 healthy volunteers, 5 high-risk volunteers, and 31 HIV-infected outpatients was assayed for cytokine production in response to endotoxin (LPS) or staphylococcal enterotoxin B (SEB) in the presence or absence of 100 ng/mL Filgrastim. LPSinducible blood cytokine release of HIV-infected patients was not different from that of normal or high-risk volunteers. The suppressive effect of Filgrastim on LPS-inducible blood tumor necrosis factor-a and interferon-g formation in normal volunteers was not found in HIV-infected patients. Patients with advanced HIV infection showed reduced IL-2 and IL-4 release in the presence of SEB. In the presence of Filgrastim, IL-2 production was partially restored.Filgrastim (granulocyte colony-stimulating factor, r-metHuG-HIV-infected patients are known to develop major defects of the immune signaling system [20], in particular of the cytokine-CSF) is a hematopoietic growth factor primarily of neutrophilic granulocytes. It is used clinically to treat neutropenia due to mediator system. Some proinflammatory cytokines, such as tumor necrosis factor (TNF)-a and interferon (IFN)-g, are myelosuppressive chemo-or radiation therapy, severe chronic neutropenia, human immunodeficiency virus (HIV) infection, and found to be increased [5, 21 -23] and have been implicated in the promotion of viral replication [24]. More recently, lymphoother diseases [1]. HIV-infected patients may develop neutropenia because of the myelosuppressive effects of HIV or because kines, such as interleukin (IL)-2, have been thought to play an important role in the progression of HIV infection to AIDS. of some of the drugs used to treat these patients [2]. Both HIVinfected patients and HIV-infected leukocytes have shown a re-IL-2 formation by CD4 T cells appears to be mandatory in maintaining CD8 T cell control of viral replication [25]. A duced ability to produce G-CSF [3][4][5]. Neutropenia appears to be a risk factor and contributes to the increased incidence of switch from Th1-type lymphokines (primarily IL-2) to Th2-type lymphokines (IL-4, IL-10) was suggested to represent the infections in neutropenic HIV-infected patients [6][7][8], and Filgrastim treatment has been shown to reverse neutropenia in HIVchange from asymptomatic HIV infection to AIDS [26]. Studies have shown that G-CSF has a widespread effect as infected patients and to decrease infection [9][10][11][12][13][14]. A number of functional defects of neutrophils have been reported for HIVan immunomodulator controlling the functions and activity of mature neutrophilic granulocytes [27, 28] and has profound infected patients [15][16][17] that could be reversed by Filgrastim antiinflammatory effects on m...

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Cytokines in HIV infection

Cited by 29 publications

References 26 publications

Antitumorigenic effects of HIV protease inhibitor ritonavir: inhibition of Kaposi sarcoma

Antitumorigenic effects of HIV protease inhibitor ritonavir: inhibition of Kaposi sarcoma

Cytokine signals propagate through the brain

Filgrastim Restores Interleukin‐2 Production in Blood from Patients with Advanced Human Immunodeficiency Virus Infection

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