Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
2006-5-19
pubmed:abstractText
Induction of stroke not only produces local ischemia and brain damage, but also has profound effects on peripheral immune responses. In the current study, we evaluated effects on spleen and blood cells 4 days after stroke induction. Surprisingly, there was a less inflammatory cytokine profile in the middle cerebral artery occlusion-affected right brain hemisphere at 96 h compared with earlier time points. Moreover, our results demonstrate that stroke leads to splenic atrophy characterized by a reduction in organ size, a drastic loss of splenocyte numbers, and induction of annexin V+ and TUNEL+ cells within the spleen that are in the late stages of apoptosis. The consequence of this process was to reduce T cell proliferation responses and secretion of inflammatory cytokines, resulting in a state of profound immunosuppression. These changes produced a drastic reduction in B cell numbers in spleen and blood, and a novel increase in CD4+FoxP3+ regulatory T cells. Moreover, we detected a striking increase in the percentage of nonapoptotic CD11b+ VLA-4-negative macrophages/monocytes in blood. Immunosuppression in response to brain injury may account for the reduction of inflammatory factors in the stroke-affected brain, but also potentially could curtail protective immune responses in the periphery. These findings provide new evidence to support the contention that damage to the brain caused by cerebral ischemia provides a powerful negative signal to the peripheral immune system that ultimately induces a drastic state of immunosuppression caused by cell death as well as an increased presence of CD4+FoxP3+ regulatory T cells.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
176
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
6523-31
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:16709809-Animals, pubmed-meshheading:16709809-Antigens, CD11b, pubmed-meshheading:16709809-Atrophy, pubmed-meshheading:16709809-Brain, pubmed-meshheading:16709809-Brain Ischemia, pubmed-meshheading:16709809-Cell Death, pubmed-meshheading:16709809-Chemokines, pubmed-meshheading:16709809-Cytokines, pubmed-meshheading:16709809-Forkhead Transcription Factors, pubmed-meshheading:16709809-Infarction, Middle Cerebral Artery, pubmed-meshheading:16709809-Leukocyte Count, pubmed-meshheading:16709809-Macrophages, pubmed-meshheading:16709809-Male, pubmed-meshheading:16709809-Mice, pubmed-meshheading:16709809-Mice, Inbred C57BL, pubmed-meshheading:16709809-Spleen, pubmed-meshheading:16709809-T-Lymphocytes, Regulatory, pubmed-meshheading:16709809-Thymus Gland, pubmed-meshheading:16709809-Up-Regulation
pubmed:year
2006
pubmed:articleTitle
Splenic atrophy in experimental stroke is accompanied by increased regulatory T cells and circulating macrophages.
pubmed:affiliation
Neuroimmunology Research, Veterans Affairs Medical Center, Portland, OR 97239, USA. offnerva@ohsu.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Research Support, N.I.H., Extramural