736 research outputs found
What is the blood-brain barrier (not)?
No full textIn 1900, summarizing his experiments with toxins and Ehrlich's earlier observations with intravital dyes, the Berlin physician Lewandowski concluded that "brain capillaries must hold back certain molecules". Illustrating this phenomenon with persuasive beauty, the subsequently evolving metaphor of a 'Bluthirnschranke' (blood-brain barrier, BBB) gained wide acceptance, but the extension of its meaning into the context of inhibiting leukocyte recruitment into the brain is imprecise. On the basis of the original work by Ehrlich, Lewandowski and Goldmann we re-define the BBB as a capillary barrier for solutes, and clarify that leukocyte recruitment requires two differentially regulated steps: (i) passage across postcapillary venules into Virchow-Robin spaces, and (ii) subsequent progression across the glia limitans into the neuropil. We propose that the second step frequently involves perivascular antigen-recognition and the induction of ectoenzymes, for example matrix metalloproteinases (MMPs)
What is immune privilege (not)?
No full textThe ‘immune privilege’ of the central nervous system (CNS) is indispensable for damage limitation during inflammation in a sensitive organ with poor regenerative capacity. It is a longstanding notion which, over time, has acquired several misconceptions and a lack of precision in its definition. In this article, we address these issues and re-define CNS immune privilege in the light of recent data. We show how it is far from absolute, and how it varies with age and brain region. Immune privilege in the CNS is often mis-attributed wholly to the blood–brain barrier. We discuss the pivotal role of the specialization of the afferent arm of adaptive immunity in the brain, which results in a lack of cell-mediated antigen drainage to the cervical lymph nodes although soluble drainage to these nodes is well described. It is now increasingly recognized how immune privilege is maintained actively as a result of the immunoregulatory characteristics of the CNS-resident cells and their microenvironment
Ingo Plag, Word-Formation in English (2
No full text1. General observations Ingo Plag is Professor of English Linguistics at Heinrich-Heine-Universität Düsseldorf. He has published articles in specialized journals like Linguistics, Language or English Language and Linguistics and in works like the Yearbook of Morphology [2001], Word-Formation: An International Handbook of the Languages of Europe [2016] or Word Knowledge and Word Usage: A Cross-Disciplinary Guide to the Mental Lexicon [2017]. He is the author of Morphological Productivity: Stru..
Innovation reziprok. Intermediäre Kooperation zwischen akademischer Forschung und Industrie
No full textSchulz-Schaeffer I, Jonas M, Malsch T. Innovation reziprok. Intermediäre Kooperation zwischen akademischer Forschung und Industrie. In: Rammert W, Bechmann G, eds. Innovation – Prozesse, Produkte, Politik. Technik und Gesellschaft. Vol Jahrbuch 9. Frankfurt am Main: Campus-Verlag; 1997: 91-124
Vascular, glial, and lymphatic immune gateways of the central nervous system
No full textImmune privilege of the central nervous system (CNS) has been ascribed to the presence of a blood-brain barrier and the lack of lymphatic vessels within the CNS parenchyma. However, immune reactions occur within the CNS and it is clear that the CNS has a unique relationship with the immune system. Recent developments in high-resolution imaging techniques have prompted a reassessment of the relationships between the CNS and the immune system. This review will take these developments into account in describing our present understanding of the anatomical connections of the CNS fluid drainage pathways towards regional lymph nodes and our current concept of immune cell trafficking into the CNS during immunosurveillance and neuroinflammation. Cerebrospinal fluid (CSF) and interstitial fluid are the two major components that drain from the CNS to regional lymph nodes. CSF drains via lymphatic vessels and appears to carry antigen-presenting cells. Interstitial fluid from the CNS parenchyma, on the other hand, drains to lymph nodes via narrow and restricted basement membrane pathways within the walls of cerebral capillaries and arteries that do not allow traffic of antigen-presenting cells. Lymphocytes targeting the CNS enter by a two-step process entailing receptor-mediated crossing of vascular endothelium and enzyme-mediated penetration of the glia limitans that covers the CNS. The contribution of the pathways into and out of the CNS as initiators or contributors to neurological disorders, such as multiple sclerosis and Alzheimer's disease, will be discussed. Furthermore, we propose a clear nomenclature allowing improved precision when describing the CNS-specific communication pathways with the immune system
CD11c-positive cells from brain, spleen, lung, and liver exhibit site-specific immune phenotypes
No full textFailure of perivascular drainage of β-amyloid in cerebral amyloid angiopathy
No full textIn Alzheimer's disease, amyloid-β (Aβ) accumulates as insoluble plaques in the brain and deposits in blood vessel walls as cerebral amyloid angiopathy (CAA). The severity of CAA correlates with the degree of cognitive decline in dementia. The distribution of Aβ in the walls of capillaries and arteries in CAA suggests that Aβ is deposited in the perivascular pathways by which interstitial fluid drains from the brain. Soluble Aβ from the extracellular spaces of gray matter enters the basement membranes of capillaries and drains along the arterial basement membranes that surround smooth muscle cells toward the leptomeningeal arteries. The motive force for perivascular drainage is derived from arterial pulsations combined with the valve effect of proteins present in the arterial basement membranes. Physical and biochemical changes associated with arteriosclerosis, aging and possession of apolipoprotein E4 genotype lead to a failure of perivascular drainage of soluble proteins, including Aβ. Perivascular cells associated with arteries and the lymphocytes recruited in the perivenous spaces contribute to the clearance of Aβ. The failure of perivascular clearance of Aβ may be a major factor in the accumulation of Aβ in CAA and may have significant implications for the design of therapeutics for the treatment of Alzheimer's disease
CD11c-positive cells from brain, spleen, lung, and liver exhibit site-specific immune phenotypes
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