52 research outputs found
Immunohistochemical identification of T-lymphocytes in the central nervous system of patients with multiple sclerosis and subacute sclerosing panencephalitis.
T-lymphocytes were identified in frozen brain sections derived from patients with chronic inflammatory disorders of the CNS by using a specific heteroantiserum and the unlabelled antibody enzyme method. Clusters of T-cells were found in post-mortem material of cases with multiple sclerosis (MS) and subacute sclerosing penencephalitis (SSPE). The results suggest that T-lymphocytes are involved in the pathogenesis of both MS and SSPE
Immunohistochemical analysis of CDX2 expression in normal choroid plexus epithelium and choroid plexus tumors
Background: The Wnt and BMP signaling
pathways are involved in the morphogenesis of both
gastrointestinal and choroid plexus epithelium. In the
intestine, Wnt signaling represses the expression of the
tumor suppressor gene CDX2 via SOX9, a transcription
factor, which is also expressed in the choroid plexus.
Recently, an inverse correlation between CDX2
expression and tumor grade, tumor stage and lymph
node metastasis in colorectal adenocarcinomas has been
reported. Besides intestinal tissues, expression of CDX2
has also been reported in various other epithelial tissues
and carcinomas. To date, no data exist on expression of
CDX2 in normal and neoplastic choroid plexus
epithelium. Aim: To investigate CDX2 expression in
normal and neoplastic choroid plexus. Materials and
Methods: Paraffin-embedded samples from 60 normal
choroid plexus, including 23 fetal tissue samples and
from 65 choroid plexus tumors (47 choroid plexus
papillomas WHO grade I, 16 atypical choroid plexus
papillomas and 2 choroid plexus carcinomas WHO
grade III) were examined by immunohistochemistry.
Samples from normal choroid plexus were collected
from 45 autopsy cases and from 15 neurosurgical
specimens. Results: Normal and neoplastic choroid
plexus lacked CDX2 expression. Conclusion: In our
series, immunohistochemistry shows no evidence for a
role of CDX2 in development or differentiation of
normal choroid plexus from the 9th gestational week
until adulthood. Since choroid plexus tumors reliably
lack CDX2 immunoreactivity, this marker may be helpful in distinguishing cerebral metastases from
CDX2-positive adenocarcinomas and choroid plexus
neoplasms
Expression of integrins αvβ3 and αvβ5 and their ligands in primary and secondary central nervous system neoplasms
Aims: To study the expression of integrins αvβ3 and αvβ5 and their ligands in tumour, stroma and endothelial cells from human glioblastoma and CNS metastases from breast, lung and skin tumours. Methods and results: Integrin and integrin ligand expression was quantified in frozen tumour surgical specimens (15 glioblastomas and breast carcinoma metastases as well as 16 lung carcinoma and melanoma metastases) using immunohistochemistry. Gene expression profiles were evaluated in glioblastomas (n=424) and in normal brain (n=11). Overall, αvβ3 expression was more common than αvβ5 except in tumours derived from lung. αvβ3 expression was most frequent in glioblastomas and melanoma metastases. Most lung-derived tumours expressed αvβ5 but expression was less frequent in other tumours; about 20% of breast-derived tumours strongly expressed αvβ5. Melanoma-derived tumours did not express αvβ5. Expression of integrin ligands vitronectin, fibrinogen, fibronectin and osteopontin was variable between tumours, although most tumours expressed the ligands to some extent. Marked αvβ3, but not αvβ5, expression was common in stroma of CNS metastases. In blood vessels, αvβ3 expression was more frequent than αvβ5 and more pronounced in CNS metastases than in glioblastomas. Integrin ligand expression occurred in blood vessels in most tumours. In glioblastomas, mRNA expression of αvβ3, αvβ5, osteopontin and fibronectin were significantly upregulated over normal brain. Conclusions: Overall, we report distinct and heterogeneous patterns of integrin expression in primary and secondary brain tumours that may be relevant to the future development of integrin-targeting therapeutic approaches to brain tumours
De novo expression of the hemoglobin scavenger receptor CD163 by activated microglia is not associated with hemorrhages in human brain lesions
The main function of CD163 (hemoglobin
scavenger receptor) is to bind the hemoglobinhaptoglobin
complex, thereby mediating extravasal
hemolysis. However, CD163 also has an
antiinflammatory function. After CD163-mediated
endocytosis, hemoglobin is catabolized further by
hemeoxygenase 1 (HO-1). Previously, we found
expression of HO-1 to be restricted to microglia/
macrophages at sites of hemorrhages in human traumatic
and ischemic brain lesions. We now investigated if
CD163 expression is also correlated with hemorrhages
in brain lesions. Methods. Autopsy brain tissue from 44
cases with hemorrhagic brain lesions (32 traumatic brain
injuries/TBI, 12 intracerebral bleedings/ICB), 56 nonhemorrhagic
brain lesions (30 ischemias, 26 hypoxias)
and 6 control brains were investigated. The post injury
survival times ranged from a few minutes to 60 months.
Results. In controls, single perivascular monocytes
expressed CD163, but only single CD163+ microglia
were found in 3/6 cases. CD163+ cells in the
parenchyma (activated microglia/macrophages)
increased significantly within 24 hours after trauma and
ischemia and within 1-7 days following ICB or hypoxia.
Overall, significantly lower and higher levels of
parenchymal CD163+ cells occurred in hypoxia and
ischemia, respectively. Perivascular CD163+ cells also
increased significantly in all pathological conditions. In
areas remote from circumscribed brain lesions (TBI,
ICB, ischemia), significant changes were only found in
ICB and ischemia. Conclusions. De novo expression of
CD163 by activated microglia/macrophages and
CD163+ infiltrating monocytes are neither restricted to
nor predominant in hemorrhagic brain lesions. Thus, the
antiinflammatory function of CD163 probably
predominates, both in hemorrhagic and non-hemorrhagic
brain lesions and points to possible immunomodulatory
treatment strategies targeting CD16
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