Origin of Brain Macrophages in the Mouse

Konigsmark, Bruce W.; Sidman, Richard L.

doi:10.1097/00005072-196310000-00006

Cited by 257 publications

(40 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Whereas it is generally accepted that bone marrow origin cells are responsible for continued replacement of macrophages in tissues such as lung and liver (33,34), the origin and turnover of CNS phagocytes is less well understood. There is evidence that murine brain contains a resident population of phagocytic cells that are of bone marrow origin (35,36). To what extent there is postembryologic renewal of cells within the CNS from the marrow is not well established.…”

Section: Discussionmentioning

confidence: 99%

Bone marrow transplantation in canine mucopolysaccharidosis I. Effects within the central nervous system.

Shull¹,

Hastings²,

Selcer³

et al. 1987

J. Clin. Invest.

View full text Add to dashboard Cite

Five dogs with mucopolysaccharidosis I, a model of human Hurler/Scheie syndrome, were transplanted with marrow from phenotypically normal littermates at 5 mo of age. At 3 and 9 mo posttransplantation, biopsies of cerebral cortex, liver, and cerebrospinal fluid were obtained. The a-L-iduronidase levels in these tissues were 0.8-7.4, 26-45, and 6.3-14.9% of the paired donor tissues, respectively. Although iduronidase was present in relatively low levels in the recipients' brains and cerebrospinal fluid at both biopsy times, reduction in brain glycosaminoglycan (GAG) was comparable to that observed in liver. Ultrastructural studies of cells within the transplanted dogs' brains showed less lysosomal distension and storage product than in affected, nontransplanted, littermate controls. The most marked clearing of stored GAG was in cells surrounding blood vessels, but decreased lysosomal storage in neurons and glial cells was also observed. Urinary GAG excretion also decreased to near normal levels by 5 mo posttransplantation.

show abstract

Section: Discussionmentioning

confidence: 99%

Bone marrow transplantation in canine mucopolysaccharidosis I. Effects within the central nervous system.

Shull¹,

Hastings²,

Selcer³

et al. 1987

J. Clin. Invest.

View full text Add to dashboard Cite

show abstract

“…Stavrou et al (1977) (Konigsmark & Sidman, 1963;Roessmann & Friede, 1968;Oehmichen & Gencic, 1975;Fujita & Katamura, 1976). It therefore seems probable that many of the tumourinfiltrating macrophages found in the present study were also derived from blood monocytes.…”

Section: Discussionmentioning

confidence: 99%

“…Autoradiographic studies have provided some evidence that the macrophage-like cells in normal brain probably arise in the marrow (Roessmann & Friede, 1968) and subsequently become circulating blood monocytes (Konigsmark & Sidman, 1963) -not unlike the migratory route of the macrophage into the damaged brain.…”

Section: Discussionmentioning

confidence: 99%

Lymphoreticular cells in human brain tumours and in normal brain

Phillips¹,

Eremin²,

Anderson³

1982

Br J Cancer

View full text Add to dashboard Cite

Summary.-The present investigation, using various rosetting assays of cell suspensions prepared by mechanical disaggregation or collagenase digestion, demonstrated lymphoreticular cells in human normal brain (cerebral cortex and cerebellum) and in malignant brain tumours. The study revealed T and B lymphocytes and their subsets (bearing receptors for Fc(IgG) and C3) in 5/14 glioma suspensions, comprising < 15% of the cell population. Between 20-60% of cells in tumour suspensions morphologically resembled macrophages and s75%0 of these cells formed strong rosettes.Lymphocytes were not found in cancer-free (putatively normal) brain. Macrophages and the smaller "microglial cells" (both phagocytic, staining with sudan black, and expressing Fc(IgG) and C3 receptors) were found in normal brain in numbers similar to those in tumour suspensions, but with less rosetting avidity. These cells may be part of an immunological defence mechanism.

show abstract

“…However, this hypothesis has not been confirmed. Currently, microglial cells are widely believed to originate in the mesoderm from myeloid precursors produced in the yolk sack and, later on, in haematopoietic organs (liver and bone marrow) (Konigsmark & Sidman, 1963;Ling, 1981;Hickey & Kimura, 1988;Hutchins et al 1990;Chan et al 2007). Mononuclear phagocytes penetrate the subpial brain during early embryonic development, before vessel development within the brain parenchyma (Choi, 1981;Cuadros et al 1993;Ling & Wong, 1993;Andjelkovic et al 1998).…”

Section: Introductionmentioning

confidence: 99%

Early microglial colonization of the human forebrain and possible involvement in periventricular white‐matter injury of preterm infants

et al. 2010

View full text Add to dashboard Cite

Amoeboid microglial subpopulations visualized by antibodies against ionized calcium-binding adapter molecule 1, CD68, and CD45 enter the forebrain starting at 4.5 postovulatory or gestational weeks (gw). They penetrate the telencephalon and diencephalon via the meninges, choroid plexus, and ventricular zone. Early colonization by amoeboid microglia-macrophages is first restricted to the white matter, where these cells migrate and accumulate in patches at the junctions of white-matter pathways, such as the three junctions that the internal capsule makes with the thalamocortical projection, external capsule and cerebral peduncle, respectively. In the cerebral cortex anlage, migration is mainly radial and tangential towards the immature white matter, subplate layer, and cortical plate, whereas pial cells populate the prospective layer I. A second wave of microglial cells penetrates the brain via the vascular route at about 12-13 gw and remains confined to the white matter. Two main findings deserve emphasis. First, microglia accumulate at 10-12 gw at the cortical plate-subplate junction, where the first synapses are detected. Second, microglia accumulate in restricted laminar bands, most notably around 19-30 gw, at the axonal crossroads in the white matter (semiovale centre) rostrally, extending caudally in the immature white matter to the visual radiations. This accumulation of proliferating microglia is located at the site of white-matter injury in premature neonates. The spatiotemporal organization of microglia in the immature white and grey matter suggests that these cells may play active roles in developmental processes such as axonal guidance, synaptogenesis, and neurodevelopmental apoptosis as well as in injuries to the developing brain, in particular in the periventricular white-matter injury of preterm infants.

show abstract

Origin of Brain Macrophages in the Mouse

Cited by 257 publications

References 0 publications

Bone marrow transplantation in canine mucopolysaccharidosis I. Effects within the central nervous system.

Bone marrow transplantation in canine mucopolysaccharidosis I. Effects within the central nervous system.

Lymphoreticular cells in human brain tumours and in normal brain

Early microglial colonization of the human forebrain and possible involvement in periventricular white‐matter injury of preterm infants

Contact Info

Product

Resources

About