Monoclonal antibody to macrophages (EMB/11) labels macrophages and microglial cells in human brain.

Esiri, M M; McGee, J O

doi:10.1136/jcp.39.6.615

Cited by 100 publications

(37 citation statements)

References 11 publications

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“…Occasional colocalization of CD11c with C1qRp was observed and may represent dendritic cells that have been shown to express C1qRp in the rat (25). Similar experiments in which the anti-C1qRp mAb BIIG-4 was used in combination with polyclonal rabbit anti-␣-1-antichymotrypsin, a monocyte/macrophage marker (26,27), confirmed the absence of C1qRp on macrophages. The ␣-1-antichymotrypsin was observed to be expressed by macrophages in tonsil, whereas C1qRp expression was mainly restricted to endothelial cells on both large and small blood vessels (Fig.…”

Section: C1qrp/cd93 Is Not Expressed By Macrophages In Human Tissue supporting

confidence: 56%

Human C1qRp Is Identical with CD93 and the mNI-11 Antigen But Does Not Bind C1q

McGreal

Ikewaki

Akatsu

et al. 2002

The Journal of Immunology

106

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It has been suggested that the human C1qRp is a receptor for the complement component C1q; however, there is no direct evidence for an interaction between C1q and C1qRp. In this study, we demonstrate that C1q does not show enhanced binding to C1qRp-transfected cells compared with control cells. Furthermore, a soluble recombinant C1qRp-Fc chimera failed to interact with immobilized C1q. The proposed role of C1qRp in the phagocytic response in vivo is also unsupported in that we demonstrate that this molecule is not expressed by macrophages in a variety of human tissues and the predominant site of expression is on endothelial cells. Studies on the rodent homolog of C1qRp, known as AA4, have suggested that this molecule may function as an intercellular adhesion molecule. Here we show that C1qRp is the Ag recognized by several previously described mAbs, mNI-11 and two anti-CD93 Abs (clones X2 and VIMD2b). Interestingly, mNI-11 (Fab′) has been shown to promote monocyte-monocyte and monocyte-endothelial cell adhesive interactions. We produced a recombinant C1qRp-Fc chimera containing the C-type lectin-like domain of C1qRp and found specific binding to vascular endothelial cells in sections of inflamed human tonsil, indicating the presence of a C1qRp ligand at this site. This interaction was Ca2+ independent and was not blocked by our anti-C1qRp mAb BIIG-4, but was blocked by the proadhesive mAb mNI-11. Collectively, these data indicate that C1qRp is not a receptor for C1q, and they support the emerging role of C1qRp (here renamed CD93) in functions relevant to intercellular adhesion.

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Section: C1qrp/cd93 Is Not Expressed By Macrophages In Human Tissue supporting

confidence: 56%

Human C1qRp Is Identical with CD93 and the mNI-11 Antigen But Does Not Bind C1q

McGreal

Ikewaki

Akatsu

et al. 2002

The Journal of Immunology

106

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“…Since EBM11 is a panmacrophage marker (CD68) that recognizes human microglial cells [3] in addition to peripheral macrophages, the microglial cells stained by EBM11 could account for the differences observed between the two mabs concerning the proportion of positive cells. Indeed, other workers recently demonstrated a microglial cells activation in glioma tissues [20].…”

Section: Discussionmentioning

confidence: 97%

Immune infiltrates and cytokines in gliomas

et al. 1996

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Frozen sections of 21 gliomas were analysed to characterize inflammatory infiltrating cells, HLA-DR antigen expression and cytokine secretion. Mononuclear cells infiltrating the tumours were mostly macrophages, which were detected in 100% of cases, and expressed HLA-DR antigens. Lymphocytes were less frequently seen and expressed the CD8 phenotype. Interleukin-1 beta (IL-1 beta) and Interleukin-6 (IL-6), two cytokines mainly produced by activated cells of the macrophage lineage, were demonstrated especially in neoplastic astrocytes. IL-1 beta immunoreactivity was detected in all tumours, and was prevalent in more anaplastic gliomas; IL-6 was found in anaplastic gliomas and in glioblastomas. IL-1 receptors were expressed by both infiltrating macrophages and neoplastic astrocytes in the gliomas analysed. These findings suggest that cytokine production in gliomas seems not related to immune reactions against the tumour and their synthesis by anaplastic astrocytes could follow an unregulated activation of many metabolic processes after neoplastic transformation.

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“…Cluster of differentiation 68 (CD68) is specifically expressed in the lysosomal granules of macrophages from various human tissues and of microglial cells in the developing and in the adult brain (Esiri and McGee, 1986;Rezaie and Male, 1997). Macrosialin is the murine homolog of CD68.…”

Section: Immunostainingmentioning

confidence: 99%

Pattern of invasion of the embryonic mouse spinal cord by microglial cells at the time of the onset of functional neuronal networks

Rigato

Buckinx

Le-Corronc

et al. 2011

Glia

131

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Microglial cells invade the central nervous system during embryonic development, but their developmental functional roles in vivo remain largely unknown. Accordingly, their invasion pattern during early embryonic development is still poorly understood. To address this issue, we analyzed the initial developmental pattern of microglial cell invasion in the spinal cord of CX3CR1-eGFP mouse embryos using immunohistochemistry. Microglial cells began to invade the mouse embryonic spinal cord at a developmental period corresponding to the onset of spontaneous electrical activity and of synaptogenesis. Microglial cells reached the spinal cord through the peripheral vasculature and began to invade the parenchyma at 11.5 days of embryonic age (E11.5). Remarkably, at E12.5, activated microglial cells aggregated in the dorsolateral region close to terminals of dying dorsal root ganglia neurons. At E13.5, microglial cells in the ventral marginal zone interacted with radial glial cells, whereas ramified microglial cells within the parenchyma interacted with growing capillaries. At this age, activated microglial cells (Mac-2 staining) also accumulated within the lateral motor columns at the onset of the developmental cell death of motoneurons. This cell aggregation was still observed at E14.5, but microglial cells no longer expressed Mac-2. At E15.5, microglial cells were randomly distributed within the parenchyma. Our results provide the essential basis for further studies on the role of microglial cells in the early development of spinal cord neuronal networks in vivo.

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Monoclonal antibody to macrophages (EMB/11) labels macrophages and microglial cells in human brain.

Cited by 100 publications

References 11 publications

Human C1qRp Is Identical with CD93 and the mNI-11 Antigen But Does Not Bind C1q

Human C1qRp Is Identical with CD93 and the mNI-11 Antigen But Does Not Bind C1q

Immune infiltrates and cytokines in gliomas

Pattern of invasion of the embryonic mouse spinal cord by microglial cells at the time of the onset of functional neuronal networks

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