Linked Life Data

16247182

Source:http://linkedlifedata.com/resource/pubmed/id/16247182

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2005-10-25
pubmed:abstractText
Immunity is required to eliminate dangerous or degenerated material and to support regeneration, but also causes significant parenchymal damage. In the eye and the brain, in which cornea and lens poorly regenerate and neurons are hardly replaceable, early transplantation experiments demonstrated remarkable tolerance to various grafts. This "immunologically privileged status" (Billingham and Boswell, 1953) may reflect evolutionary pressure to downmodulate certain actions of immune cells within particularly vulnerable tissues. As an example, tolerating certain "neurotrophic" viruses may often be a more successful strategy for survival than the elimination of all infected neurons. While several constitutive and inducible signals maintaining or re-establishing immune tolerance within the brain have been identified, it has also become evident that the resulting anti-inflammatory environment limits certain beneficial effects of neuroinflammation such as neurotrophin secretion or glutamate buffering by T-cells and the clearance of growth-inhibiting myelin or amyloid. Following spinal cord injury, the costs and benefits of neuroinflammation seem to come close because enhancing as well as suppressing innate or adaptive immunity caused amelioration and aggravation of functional regeneration in similar experiments. Evaluating such balances has also begun in (animal models of) Alzheimer's disease, central nervous system trauma, and stroke, and the appreciation of the beneficial side of neuroinflammation has caused a rethinking of the ill-defined use of immune suppressants. As dual roles for individual molecules have been recognized (Merrill and Benveniste, 1996), we are uncovering an already fine-tuned system, but the challenge remains to further support beneficial immune cascades without causing additional damage, and vice versa.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1535-1084
pubmed:author
pubmed:issnType
Print
pubmed:volume
7
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
217-28
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
Failed central nervous system regeneration: a downside of immune privilege?
pubmed:affiliation
Center for Anatomy, Institute of Cell Biology and Neurobiology, Department of Experimental Neuroimmunology, Charité-Universitätsmedizin Berlin, Schumannstr, 20/21 10098 Berlin, Germany. ingo.bechmann@charite.de
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't