Inhibition of interleukin‐6‐induced human immunodeficiency virus type 1 expression by anti‐GP130 monoclonal antibody

Okamoto, Masato; Yasukawa, Kiyoshi; Katsuura, K.; Baba, Masanori

doi:10.1080/15216549700204541

IUBMB Life

1997

DOI: 10.1080/15216549700204541

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Inhibition of interleukin‐6‐induced human immunodeficiency virus type 1 expression by anti‐GP130 monoclonal antibody

Masato Okamoto

Kiyoshi Yasukawa

K. Katsuura

et al.

Abstract: Interleukin 6 (IL‐6) has been reported to upregulate the expression of human immuno‐deficiency virus type 1 (HIV‐1) in infected monocyte/macrophages. Since IL‐6 signal is transduced through the membrane glycoprotein gp130, we investigated the inhibitory effect of anti‐gp130 monoclonal antibody (mAb) on IL‐6‐induced viral expression in monocytic cell lines latently infected with HIV‐I. IL‐6 significantly induced the expression of HIV‐1 in U1 cells, whereas it had no effect in OM‐10.1 cells. Flow cytometric anal… Show more

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2008

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“…46 Monocytic cell lines expressing IL-6R secreted more IL-6, which up-regulated HIV-1 expression, and antibodies to IL-6R inhibited IL-6-induced HIV-1 expression. 47 This suggests that increased expression of IL-6 and IL-6R can potentiate viral-induced effects on the brain endothelium and contribute to For personal use only. on May 11, 2018. by guest www.bloodjournal.org From HIV-induced BBB dysfunction.…”

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STAT1 signaling modulates HIV-1–induced inflammatory responses and leukocyte transmigration across the blood-brain barrier

Chaudhuri

Yang

Gendelman

et al. 2008

Blood

128

156

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The relationship among neuroinflammation, blood-brain barrier (BBB) dysfunction, and progressive HIV-1 infection as they affect the onset and development of neuroAIDS is incompletely understood. IntroductionHuman immunodeficiency virus type 1 (HIV-1) infection of the central nervous system (CNS) commonly results in behavioral, motor, and cognitive impairments. [1][2][3] Although disease severity and progression has slowed, in part, as a result of antiretroviral therapy, 76% to 83% of brain autopsies continue to show observable neuropathological abnormalities. [4][5][6] Disease pathology ranges from mild brain atrophy and gliosis to robust viral replication, multinucleated giant cell formation, astrogliosis and microgliosis, myelin pallor, and neuronal loss. 7,8 These pathological findings are collectively termed HIV-1 encephalitis (HIVE). HIVE is a common correlate to the later stages of behavioral, motor, neuropsychiatric, and neurologic consequences of disease termed HIV-1-associated dementia (HAD) (for recent reviews, see McArthur 1 ; Grant et al 2 ; Ghafouri 3 ). HIVE is fueled by viral infection and immune activation of brain mononuclear phagocytes (MPs: blood-derived perivascular macrophages and microglia). 9 Such MP-and virus-associated neuroinflammation promotes monocyte trafficking across the bloodbrain barrier (BBB), MP infiltration into the CNS, and neurodegeneration. [10][11][12] Thus, dysfunction of the BBB is one critical feature of HIV-1 neuropathogenesis.Brain microvascular endothelial cells, a major component of BBB function and integrity, are connected by tight junctions (TJs) that limit paracellular flux and restrict permeability. 13 Indeed, under normal physiologic conditions, the brain endothelium functions as an interface between the blood and the brain parenchyma, strictly regulating influx of ions, molecules, and leukocytes into the CNS. Nonetheless, in disease, a variety of environmental, toxic, degenerative, and microbial insults could cause BBB breakdown. 12,14 Such a breakdown occurs during progressive HIV-1 infection 12,[15][16][17] and was documented in laboratory, animal models, human clinical observations, and autopsy studies. 10,[16][17][18][19][20] Underlying mechanisms of BBB dysfunction and how it affects ongoing disease are incompletely understood. 1,12,14 Dysfunction of the BBB enhances penetration of cell-free virus, ingress of activated HIV-1-infected monocytes across the BBB, accumulation of MP in the CNS, and spread of the virus to neighboring microglia and astrocytes. 15,21 Thus, BBB breech is commonly associated with accelerated disease and the development of behavioral and cognitive deficits that are signatures of HAD. 1,16 Based on these observations, the elucidation of the signaling pathways mediating BBB compromise can prove important for understanding disease mechanisms and development of new therapies.Signal transducers and activators of transcription (STATs) proteins are latent cytoplasmic transcription factors that are phosphorylated by Janus kinases (JAKs) in...

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mentioning

confidence: 99%

STAT1 signaling modulates HIV-1–induced inflammatory responses and leukocyte transmigration across the blood-brain barrier

Chaudhuri

Yang

Gendelman

et al. 2008

Blood

128

156

View full text Add to dashboard Cite

show abstract

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Inhibition of interleukin‐6‐induced human immunodeficiency virus type 1 expression by anti‐GP130 monoclonal antibody

Cited by 1 publication

References 5 publications

STAT1 signaling modulates HIV-1–induced inflammatory responses and leukocyte transmigration across the blood-brain barrier

STAT1 signaling modulates HIV-1–induced inflammatory responses and leukocyte transmigration across the blood-brain barrier

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