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Jack P. Antel

Researcher at Montreal Neurological Institute and Hospital

Publications -  540
Citations -  49656

Jack P. Antel is an academic researcher from Montreal Neurological Institute and Hospital. The author has contributed to research in topics: Multiple sclerosis & Microglia. The author has an hindex of 105, co-authored 519 publications receiving 43950 citations. Previous affiliations of Jack P. Antel include Université de Montréal & Howard Hughes Medical Institute.

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Axonal Loss and Neurofilament Phosphorylation Changes Accompany Lesion Development and Clinical Progression in Multiple Sclerosis

TL;DR: The long‐term sequelae of inflammatory demyelination on neurons and axons in multiple sclerosis are poorly known and the prognosis for these sequelae is poor.
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The role of MRI in clinical trials of multiple sclerosis: comparison of image processing techniques.

TL;DR: A conference was held, sponsored by the US and Canadian multiple sclerosis societies, to review the present status of various MRI processing strategies and their potential role in clinical trials and presents the conclusions reached and recommendations for further action that emerged.
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Regulation of Th1 and Th2 lymphocyte migration by human adult brain endothelial cells.

TL;DR: It is suggested that HBECs composing the BBB favor the migration of Th2 cells, a putative means to induce bystander suppression in the CNS, and this selectivity may help prevent activated Th1 lymphocytes, the putative CNS autoimmune disease initiating cells, from reaching the CNS parenchyma.
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HLA class II molecules (HLA-DR, -DP, -DQ) on cells in the human CNS studied in situ and in vitro.

TL;DR: Although both microglia and astrocytes are capable of expressing all HLA class II subtypes in vitro, subtype expression differs between normal and pathological states in situ, indicating selective expression may be associated with functional properties.
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Regulation of CD14 expression on human adult central nervous system-derived microglia

TL;DR: The de novo expression of CD14 by adult human CNS‐derived microglia which acquire a bipolar activated morphologic phenotype in dissociated tissue culture indicates the selective effects of molecules, likely to be present in the infected or inflamed CNS, on regulating CD14 expression and that there can be differential regulation of immune response relevant molecules expressed by activatedmicroglia.