Production, characterization, and interspecies reactivities of monoclonal antibodies against human class A macrophage scavenger receptors

Tomokiyo, Ryu Ichiro; Jinnouchi, Katsunori; Honda, Makoto; Wada, Youichiro; Hanada, Norihisa; Hiraoka, Takehisa; Suzuki, Hiroshi; Kodama, Tatsuhiko; Takahashi, Kiyoshi; Takeya, Motohiro

doi:10.1016/s0021-9150(01)00624-4

Cited by 99 publications

(82 citation statements)

References 31 publications

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“…Plasmids, however, have phosphodiester bonds, are double stranded, and entail an abundance of nucleotides likely to generate multiple CpG motifs. Similar to ssCpG-ODN, dspDNA also is taken up by macrophages and DCs, presumably via receptor-mediated endocytosis (26,27), which appears not to involve class A or B scavenger receptors (28). In this study, we show that murine conventional and pDC subsets deficient in TLR9 are unresponsive to pDNA, both in terms of cytokine production and up-regulation of costimulatory molecules.…”

Section: Discussionmentioning

confidence: 67%

Vaccination with Plasmid DNA Activates Dendritic Cells via Toll-Like Receptor 9 (TLR9) but Functions in TLR9-Deficient Mice

Spies

Hochrein

Vabulas

et al. 2003

The Journal of Immunology

187

124

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We analyzed whether the immunobiology of vaccinating plasmid DNA containing a transcription unit for OVA is influenced by immunostimulatory CpG motifs in the plasmid backbone. Indeed, plasmid DNA differentially activated in vitro myeloid and plasmacytoid dendritic cells (DCs) provided they expressed the CpG-DNA receptor, Toll-like receptor 9 (TLR9). Dependent on the DC subset, activation resulted in type 1 IFN production, while both DC subsets produced IL-6 and up-regulated expression of costimulatory molecules CD40 and CD86. In vivo, however, even upon repeated vaccination with plasmid DNA, priming of OVA-specific CTL and clonal expansion of SIINFEKL-specific CD8 T cells were equal in TLR9-positive and TLR9- or MyD88-negative mice. Overall, these results negate a dominant role of CpG-DNA/TLR9 interactions in long-term vaccination protocols.

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Section: Discussionmentioning

confidence: 67%

Vaccination with Plasmid DNA Activates Dendritic Cells via Toll-Like Receptor 9 (TLR9) but Functions in TLR9-Deficient Mice

Spies

Hochrein

Vabulas

et al. 2003

The Journal of Immunology

187

124

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“…Western blot analyses of protein lysates from PM isolated from these mouse strains were performed using Abs specific for mouse MSR1 that did not differentiate between genetic variants (13). Higher levels of MSR1 were consistently observed in B6 with respect to A/J-isolated PM (1.6-fold, p Ͻ 0.005; Fig.…”

Section: The Expression Of Msr1 Is Different Between B6 and A/j Micementioning

confidence: 99%

“…Proteins immobilized on a polyvinylidene difluoride (PVDF) membrane were quenched for 1 h with TBS-TBST (20 mM Tris, 500 mM NaCl, 0.1% Tween 20) containing 5% powdered milk, and incubated with anti-mouse MSR1 (1/5,000) for 16 h at 4°C. This Ab was raised in rabbit against a synthetic peptide (KEEQAHVEQEVKQEVR) corresponding to the ␣ helical coiled-coil domain of mouse MSR1 common to various mouse strains (13). Membranes were washed three times with TBST and incubated with HRP-conjugated anti-rabbit-IgG (1/25,000; Amersham Pharmacia Biotech) in blocking buffer for 1 h. Membranes were washed again with TBST and the signal was visualized using Super Signal West Dura (Pierce Biotechnology).…”

Section: Isolation Of Mouse Peritoneal Macrophages (Pm)mentioning

confidence: 99%

A Quantitative Trait Loci Analysis to Map Genes Involved in Lipopolysaccharide-Induced Inflammatory Response: Identification of Macrophage Scavenger Receptor 1 as a Candidate Gene

Fulton¹,

Reeves

Takeya

et al. 2006

The Journal of Immunology

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Septic shock, which is a major complication observed after trauma and other human diseases, is likely the product of a prolonged and poorly controlled systemic inflammatory response. Symptoms of sepsis can be partially reproduced by injection of bacterial LPS in mice. Differences in mortality between C57BL/6Jhigh and A/Jlow mice after LPS injection have been previously observed and correlated with differences in the inflammatory response between these two inbred strains. In the present study, we have mapped four loci responsible for differences in levels of LPS-induced IL-10, named modifier of IL-10, between the two strains. A locus within mouse chromosome 8 was confirmed using chromosome 8 consomic mice. This locus was further reduced in size by haplotype analysis and evaluated by the presence of potential candidate genes. The macrophage scavenger receptor 1 (Msr1) within this locus emerged as a candidate gene based on differences at the expression and structural levels between C57BL/6J and A/J mice. In comparison with wild-type (C57BL/6J) mice, Msr1 knockout mice displayed reduced levels of LPS-induced IL-10, but not of TNF-α or IL-6, confirming a specific role for this gene in the regulation of IL-10. These results suggest that Msr1 is involved in the regulation of the anti-inflammatory process, thus offering a new perspective on the molecular mechanisms involved in endotoxemia and sepsis.

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“…Induction of CD163 and CD204 in M2 macrophages was evaluated by means of cell-enzyme-linked immunosorbent assay and Western blot, respectively. 21,24 In the co-culture experiment, SLVL cells in 24-well plates were co-cultured with TCS-stimulated M2 macrophages or interferon-gstimulated M1 macrophages using transwell chamber dishes (Nunc, Rochester, NY, USA) for 4 or 5 days as described previously.…”

Section: Cell-cell Interactionsmentioning

confidence: 99%

M2 Macrophage/Microglial Cells Induce Activation of Stat3 in Primary Central Nervous System Lymphoma

Komohara

Horlad

Ohnishi

et al. 2011

J Clin Exp Hematopathol

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Primary central nervous system lymphoma (PCNSL) is one of the most aggressive malignant lymphomas with a median survival of less than 20∼40 months. Interest in signal transducer and activator of transcription 3 (Stat3) has increased during the past decade because Stat3 activation was found to contribute to tumor progression by inducing angiogenesis, immunosuppression, and metastasis. We previously demonstrated a significant correlation between Stat3 activation in tumor cells and infiltrating anti-inflammatory (M2) macrophages. Here, we focused on the phenotypes of infiltrating macrophages/microglial cells and Stat3 activation in PCNSL cells. The correlation of Stat3 activation or density of M2 macrophage infiltration with patient prognosis was also evaluated. We performed immunostaining for CD68, CD163, CD204, and pStat3 using paraffinembedded PCNSL specimens obtained from 43 patients. CD163 and CD204 served as markers of the M2 phenotype. Dense infiltration of CD68 + macrophages was found in all samples. High numbers of CD163 + and CD204 + M2 macrophages/microglial cells were observed in 29 and 25 cases, respectively. Stat3 activation in lymphoma cells was enhanced in the patients who showed denser infiltration of CD163 + macrophages/microglial cells in tumor tissues. In vitro co-culture experiment to investigate cell-cell interactions between macrophages and lymphoma cells found that Stat3 in lymphoma cells was strongly activated by coculture with macrophages. Numbers of CD68

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Production, characterization, and interspecies reactivities of monoclonal antibodies against human class A macrophage scavenger receptors

Cited by 99 publications

References 31 publications

Vaccination with Plasmid DNA Activates Dendritic Cells via Toll-Like Receptor 9 (TLR9) but Functions in TLR9-Deficient Mice

Vaccination with Plasmid DNA Activates Dendritic Cells via Toll-Like Receptor 9 (TLR9) but Functions in TLR9-Deficient Mice

A Quantitative Trait Loci Analysis to Map Genes Involved in Lipopolysaccharide-Induced Inflammatory Response: Identification of Macrophage Scavenger Receptor 1 as a Candidate Gene

M2 Macrophage/Microglial Cells Induce Activation of Stat3 in Primary Central Nervous System Lymphoma

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