Heterogeneity of peripheral blood monocyte populations in human immunodeficiency virus-1 seropositive patients

Abel, Pamela

doi:10.1016/0378-1097(92)90097-8

Cited by 11 publications

(12 citation statements)

References 18 publications

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“…An expansion of CD14 + CD16 + monocytes has been observed after HIV-1 infection [10]–[12] and other inflammatory conditions, while numbers of CD14 ++ monocytes do either not change [11], [13], or decrease slightly [10], in agreement with our observations. It has been assumed that CD14 + CD16 + monocytes are a distinct “proinflammatory” subset of the monocyte lineage [14].…”

Section: Discussionsupporting

confidence: 92%

Sialoadhesin (CD169) Expression in CD14+ Cells Is Upregulated Early after HIV-1 Infection and Increases during Disease Progression

et al. 2007

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BackgroundSialoadhesin (CD169, siglec-1 or Sn) is an activation marker seen on macrophages in chronic inflammatory diseases and in tumours, and on subsets of tissue macrophages. CD169 is highly expressed by macrophages present in AIDS-related Kaposi's sarcoma lesions. It is also increased on blood monocytes of HIV-1 infected patients with a high viral load despite antiretroviral treatment.Methodology/Principal FindingsWe investigated expression of sialoadhesin in untreated HIV-1 and HHV-8 infected patients, by real-time PCR and FACS analysis to establish its expression in relation to infection and disease progression. Patients analysed were either HIV-1 seroconverters (n = 7), in the chronic phase of HIV-1 infection (n = 21), or in the AIDS stage (n = 58). Controls were HHV-8 infected, but otherwise healthy individuals (n = 20), and uninfected men having sex with men (n = 24). Sialoadhesin mRNA was significantly elevated after HIV-1, but not HHV-8 infection, and a further increase was seen in AIDS patients. Samples obtained around HIV-1 seroconversion indicated that sialoadhesin levels go up early in infection. FACS analysis of PBMCs showed that sialoadhesin protein was expressed at high levels by approximately 90% of CD14+ and CD14+CD16+cells of HIV-1+ patients with a concomitant 10-fold increase in sialoadhesin protein/cell compared with uninfected controls.Conclusions/SignificanceWe have shown that sialoadhesin is induced to high levels on CD14+ cells early after HIV-1 infection in vivo. The phenotype of the cells is maintained during disease progression, suggesting that it could serve as a marker for infection and probably contributes to the severe dysregulation of the immune system seen in AIDS.

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Section: Discussionsupporting

confidence: 92%

Sialoadhesin (CD169) Expression in CD14+ Cells Is Upregulated Early after HIV-1 Infection and Increases during Disease Progression

et al. 2007

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“…In this study, we determined that NF1 patients with no overt vascular cardiovascular disease have increased numbers of circulating monocytes compared with healthy controls. Further, we identified a population of monocytes in NF1 patients that is characteristic of an activated state, including increased CD16 expression and increased size (35). The finding of increased levels of the proinflammatory cytokines IL-1β and IL-6 in plasma samples from NF1 patients supports the observation that NF1 patients have increased activated monocytes in circulation, given that, in peripheral blood, monocytes are the main producers of IL-1β and IL-6 (56).…”

Section: Figuresupporting

confidence: 63%

“…Analysis of NF1 patient peripheral blood monocytes identified a population of cells that had increased CD16 expression (CD14 dim CD16 bright ) compared with the traditional CD14 + CD16 + monocytes, a population that was not observed in peripheral blood samples from healthy controls ( Figure 6, B and C). Based on the side scatter profile, the population of CD14 dim CD16 bright monocytes, isolated from NF1 patients, was larger in size than other monocyte populations, indicating the cells had increased granularity, a characteristic of monocyte activation (35). Further, May-Grünwald-Giemsa staining of the isolated CD14 dim CD16 bright monocytes demonstrated that the cells were monocytes characterized by an extended cytoplasm and cytoplasmic vacuoles ( Figure 6A).…”

Section: Resultsmentioning

confidence: 98%

Genetic and cellular evidence of vascular inflammation in neurofibromin-deficient mice and humans

Lasater¹,

Li²,

Bessler³

et al. 2010

J. Clin. Invest.

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Neurofibromatosis type 1 (NF1) results from mutations in the NF1 tumor suppressor gene, which encodes the protein neurofibromin. NF1 patients display diverse clinical manifestations, including vascular disease, which results from neointima formation and vessel occlusion. However, the pathogenesis of NF1 vascular disease remains unclear. Vessel wall homeostasis is maintained by complex interactions between vascular and bone marrow-derived cells (BMDCs), and neurofibromin regulates the function of each cell type. Therefore, utilizing cre/lox techniques and hematopoietic stem cell transplantation to delete 1 allele of Nf1 in endothelial cells, vascular smooth muscle cells, and BMDCs alone, we determined which cell lineage is critical for neointima formation in vivo in mice. Here we demonstrate that heterozygous inactivation of Nf1 in BMDCs alone was necessary and sufficient for neointima formation after vascular injury and provide evidence of vascular inflammation in Nf1 +/-mice. Further, analysis of peripheral blood from NF1 patients without overt vascular disease revealed increased concentrations of inflammatory cells and cytokines previously linked to vascular inflammation and vasoocclusive disease. These data provide genetic and cellular evidence of vascular inflammation in NF1 patients and Nf1 +/-mice and provide a framework for understanding the pathogenesis of NF1 vasculopathy and potential therapeutic and diagnostic interventions. IntroductionNeurofibromatosis type 1 (NF1) is an autosomal dominant disorder that results from mutations in the tumor suppressor gene NF1 (1). Neurofibromin, the protein product of NF1, functions as a p21 Ras (Ras) GTPase-activating protein (GAP) to negatively regulate Ras activity (2). More than 240 different mutations have been described within the NF1 gene, all of which result in little or no protein product (3). While loss of heterozygosity has been described in primary tumor samples (4), the germline mutations that cause NF1 affect only 1 copy of the NF1 gene. Haploinsufficiency of NF1 results in disease with complete penetrance and a range of clinical complications.The most common clinical manifestations of NF1 include dermal and plexiform neurofibromas, learning deficits, and skeletal abnormalities. Vascular disease associated with NF1 is an underrecognized complication that results in increased morbidity and mortality, particularly among younger patients (5, 6). In 2001, an analysis of 3,253 death certificates of persons with NF1 indicated that the median age of death for NF1 patients was 15 years lower that of the general population (6). In this report, a diagnosis suggestive of NF1 vasculopathy was listed 7.2 times more often than expected among NF1 patients less than 30 years old at time of death and 2.2 times more often than expected among patients 30-40 years old at the time of death (6). Another study demonstrated that 2.5% of children with NF1 who had undergone brain MRI were found to have cerebrovascular system abnormalities including narrowed vessels, moyamoya, va...

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“…Reduced clearance of IgG and complement-coated cells in vivo, and reduced Pc-mediated phagocytosis of monocytes and MDM in vitro have been reported [17,18,[32][33][34]. MonoeyteHLA-DR expression in AIDS patients has been reported to be deereased [35], although more recently HLA-DR expression was reported to be increased on a subgroup oflargemonocyLes of HIV ' patients [36], A reduction in FcRIII (CD 16) has been reported in a variety of cells from HIV-infected patients, including peripheral blood lymphocytes and neutrophils, and in cells from bronchoalveolar lavage fluid [37][38][39]. The expression of FeR on monocytes isolated from HIV-infected individuals, however, has not been found to be depressed [40,41].…”

Section: Discussionmentioning

confidence: 99%

HIV-1 infection of monocyte-derived macrophages reduces Fc and complement receptor expression

Kent

Stent

Sonza

et al. 1994

Clinical and Experimental Immunology

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SUMMARYFc receptor (FcR) and complement receptor (CR) e.vpression on HIV-infectcd monocyte-derived macrophages may be an important determinant of immune function. We studied the effects of HI V-1 infection of macrophages in vitro on F'cR and CR expression. Macrophages were infected with HlV-lnv 7 days following isolation, and the expression of FcyRI-II! and CR3 were measured at intervals thereafter by flow cytometry. We found a reduction in receptor expression with the percentage of cells expressing FcRl 14 days post infection declining from 77% to 13%, FcRII fell from 96% to 85'M.. FcRIII from 45",, to 9"ii. and CR3 from 91"/;. to 67"4 14 days following infection. As these receptors are important for macrophage function, their down-modulation muy contribute to the pathogenesis of HIV-related disease.

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Heterogeneity of peripheral blood monocyte populations in human immunodeficiency virus-1 seropositive patients

Cited by 11 publications

References 18 publications

Sialoadhesin (CD169) Expression in CD14+ Cells Is Upregulated Early after HIV-1 Infection and Increases during Disease Progression

Sialoadhesin (CD169) Expression in CD14+ Cells Is Upregulated Early after HIV-1 Infection and Increases during Disease Progression

Genetic and cellular evidence of vascular inflammation in neurofibromin-deficient mice and humans

HIV-1 infection of monocyte-derived macrophages reduces Fc and complement receptor expression

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