Suppression of HIV Replication in Human Monocyte-Derived Macrophages Induced by Granulocyte/Macrophage Colony-Stimulating Factor

Matsuda, Shunji; Akagawa, Kiyoko S.; Honda, Mitsuo; Yokota, Yasuko; Takebe, Yutaka; Takemori, Toshitada

doi:10.1089/aid.1995.11.1031

Cited by 69 publications

(47 citation statements)

References 20 publications

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“…In this regard, GM-CSF is the growth factor that is traditionally used to differentiate Mos into MACs. 31,32 In the current study, we investigated CX 3 CR1 expression in circulating Mos, Mo-derived DCs or MACs using different in vitro cytokine stimulation by monitoring the phenotype of these cells at different stages in culture. Furthermore, CX 3 CR1 regulation at the transcriptional level was evaluated by mRNA analysis during Mo differentiation.…”

Section: Introductionmentioning

confidence: 99%

Differential expression of the fractalkine chemokine receptor (CX3CR1) in human monocytes during differentiation

et al. 2014

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Circulating monocytes (Mos) may continuously repopulate macrophage (MAC) or dendritic cell (DC) populations to maintain homeostasis. MACs and DCs are specialized cells that play different and complementary immunological functions. Accordingly, they present distinct migratory properties. Specifically, whereas MACs largely remain in tissues, DCs are capable of migrating from peripheral tissues to lymphoid organs. The aim of this work was to analyze the expression of the fractalkine receptor (CX 3 CR1) during the monocytic differentiation process. Freshly isolated Mos express high levels of both CX 3 CR1 mRNA and protein. During the Mo differentiation process, CX 3 CR1 is downregulated in both DCs and MACs. However, MACs showed significantly higher CX 3 CR1 expression levels than did DC. We also observed an antagonistic CX 3 CR1 regulation by interferon (IFN)-c and interleukin (IL)-4 during MAC activation through the classical and alternative MAC pathways, respectively. IFN-c inhibited the loss of CX 3 CR1, but IL-4 induced it. Additionally, we demonstrated an association between CX 3 CR1 expression and apoptosis prevention by soluble fractalkine (sCX 3 CL1) in Mos, DCs and MACs. This is the first report demonstrating sequential and differential CX 3 CR1 modulation during Mo differentiation. Most importantly, we demonstrated a functional link between CX 3 CR1 expression and cell survival in the presence of sCX 3 CL1.

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Section: Introductionmentioning

confidence: 99%

Differential expression of the fractalkine chemokine receptor (CX3CR1) in human monocytes during differentiation

et al. 2014

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“…The primary target of HIV is the CD4+ T cells and mature macrophages (Matsuda et al, 1995) and the HIV-1 transmission occurs through the mucosal tissues, which leads to the infection of these CD4+CCR5+ T cells (Weiss, 2001). Cells which do not express the surface CD4 marker are usually not susceptible to HIV infection.…”

Section: Transmission and Clinical Manifestation Of Hiv Diseasementioning

confidence: 99%

Innate, Adaptive and Intrinsic Immunity in Human Immunodeficiency Virus Infection

Perera

Saksena

2012

American Journal of Infectious Diseases

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The first line of defence of the innate immune system functions by recognizing highly conserved sets of molecular structures specific to the microbes, termed pathogen-associated molecular patterns, or PAMPs via the germ line-encoded receptors Pattern-Recognition Receptors (PRRs). In addition to the innate immune system, the vertebrates have also evolved a second line of defence termed adaptive immune system, which uses a diverse set of somatically rearranged receptors T-Cell Receptors (TCRs) and B Cell Receptors (BCRs), which have the inherent ability to effectively recognise diverse antigens. The innate and adaptive immune systems are functionally tied in with the intrinsic immunity, which comprises of endogenous antiviral factors. Thus, this effective response to diverse microbial infections, including HIV, requires a coordinated interaction at several functional levels between innate, adaptive and intrinsic immune systems. This review provides a snapshot of roles played by the innate, adaptive and the intrinsic immune systems during HIV-infection, along with discussing recent developments highlighting the genomic basis of these responses and their regulation by micro-RNA (miRNAs).

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“…We first examined whether EM derivatives ( Fig. 1) have an ability to inhibit M-tropic HIV-1 replication in macrophage colony-stimulating factor (M-CSF)-induced monocyte-derived M⌽s (M-M⌽s), which express a high level of Hck and a large isoform of C/EBP␤, are susceptible to M-tropic HIV-1 replication, and whether they form multinucleated giant cells (MGC) by cell-to-cell fusion at 4-7 d after infection (10,27). EM201 and EM703 (30 M) completely inhibited viral replication and MGC formation at 7 d after infection, while EMA, CAM, and EM202 did not ( Fig.…”

Section: Effects Of Em Derivatives On Viral Replication and Multinuclmentioning

confidence: 99%

Erythromycin derivatives inhibit HIV-1 replication in macrophages through modulation of MAPK activity to induce small isoforms of C/EBPβ

Komuro

Sunazuka

Akagawa

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

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Macrophages (MΦs) are a major source of HIV-1 especially in patients with tuberculosis. There are MΦs that are permissive and those that restrict HIV-1. Regulation of hematopoietic cell kinase (Hck) activity and selective expression of CCAAT enhancer binding protein β (C/EBPβ) isoforms greatly contribute to determine distinct susceptibility of MΦs to HIV-1. Resistance is attributable to reduced expression of Hck and augmented expression of an inhibitory small isoform of C/EBPβ. Derivatives of erythromycin A (EMA) EM201 and EM703 inhibit the replication of HIV-1 in tissue MΦs, at posttranscriptional and translational levels. We demonstrate that EM201 and EM703 convert tissue MΦs from HIV-1 susceptible to HIV-1 resistant through down-regulation of Hck and induction of small isoforms of C/EBPβ. These drugs inhibit p38MAPK activation which is expressed only in susceptible tissue MΦs. Activated CD4 + T cells stimulate the viral replication in HIV-1 resistant MΦs through down-regulation of small isoforms of C/EBPβ via activation of ERK1/2. EM201 and EM703 can inhibit the MAPK activation and inhibit the burst of viral replication produced when CD4 + T cells and MΦs interact. These EM derivatives may be highly beneficial for repression of residual HIV-1 in the lymphoreticular system of HIV-1-infected patients and offer great promise for the creation of new anti-HIV drugs for the future treatment of AIDS patients.

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Suppression of HIV Replication in Human Monocyte-Derived Macrophages Induced by Granulocyte/Macrophage Colony-Stimulating Factor

Cited by 69 publications

References 20 publications

Differential expression of the fractalkine chemokine receptor (CX3CR1) in human monocytes during differentiation

Differential expression of the fractalkine chemokine receptor (CX3CR1) in human monocytes during differentiation

Innate, Adaptive and Intrinsic Immunity in Human Immunodeficiency Virus Infection

Erythromycin derivatives inhibit HIV-1 replication in macrophages through modulation of MAPK activity to induce small isoforms of C/EBPβ

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