Linked Life Data

10477557

Source:http://linkedlifedata.com/resource/pubmed/id/10477557

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1999-10-14
pubmed:abstractText
The importance of B7 costimulation in regulating T cell expansion and peripheral tolerance suggests that it may also play a significant regulatory role in the development of autoimmune disease. It is unclear whether B7 costimulation is involved only in the expansion of autoreactive T cells in the periphery, or if it is also required for effector activation of autoreactive T cells in the target organ for mediating tissue injury and propagating autoimmune disease. In this study, the role of B7-CD28 costimulation and the relative importance of B7 costimulators for the induction and effector phases of experimental autoimmune encephalomyelitis (EAE) induced by myelin oligodendrocyte glycoprotein (MOG) peptide were examined. Wild-type, B7-1/B7-2-deficient mice, or CD28-deficient C57BL/6 mice were immunized with MOG 35-55 peptide. Mice lacking both B7-1 and B7-2 or CD28 showed no or minimal clinical signs of EAE and markedly reduced inflammatory infiltrates in the brain and spinal cord. However, mice lacking either B7-1 or B7-2 alone developed clinical and pathologic EAE that was comparable to EAE in wild-type mice, indicating overlapping functions for B7-1 and B7-2. Resistance to EAE was not due to a lack of induction of T helper type 1 (Th1) cytokines, since T cells from B7-1/B7-2(-/-) mice show reduced proliferative responses, but greater interferon gamma production compared with T cells from wild-type mice. To study the role of B7 molecules in the effector phase of the disease, MOG 35-55-specific T lines were adoptively transferred into the B7-1/B7-2(-/-) and wild-type mice. Clinical and histologic EAE were markedly reduced in B7-1/B7-2(-/-) compared with wild-type recipient mice. These results demonstrate that B7 costimulation has critical roles not only in the initial activation and expansion of MOG-reactive T cells, but also in the effector phase of encephalitogenic T cell activation within the central nervous system.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/10477557-1732276, http://linkedlifedata.com/resource/pubmed/commentcorrection/10477557-1918319, http://linkedlifedata.com/resource/pubmed/commentcorrection/10477557-2117508, http://linkedlifedata.com/resource/pubmed/commentcorrection/10477557-2273404, http://linkedlifedata.com/resource/pubmed/commentcorrection/10477557-3126227, http://linkedlifedata.com/resource/pubmed/commentcorrection/10477557-7534215, http://linkedlifedata.com/resource/pubmed/commentcorrection/10477557-7593605, http://linkedlifedata.com/resource/pubmed/commentcorrection/10477557-7655571, http://linkedlifedata.com/resource/pubmed/commentcorrection/10477557-7694362, http://linkedlifedata.com/resource/pubmed/commentcorrection/10477557-8598493, http://linkedlifedata.com/resource/pubmed/commentcorrection/10477557-8757345, http://linkedlifedata.com/resource/pubmed/commentcorrection/10477557-8766573, http://linkedlifedata.com/resource/pubmed/commentcorrection/10477557-8777719, http://linkedlifedata.com/resource/pubmed/commentcorrection/10477557-8871615, http://linkedlifedata.com/resource/pubmed/commentcorrection/10477557-8992981, http://linkedlifedata.com/resource/pubmed/commentcorrection/10477557-9075931, http://linkedlifedata.com/resource/pubmed/commentcorrection/10477557-9182689, http://linkedlifedata.com/resource/pubmed/commentcorrection/10477557-9348316, http://linkedlifedata.com/resource/pubmed/commentcorrection/10477557-9427610, http://linkedlifedata.com/resource/pubmed/commentcorrection/10477557-9743334, http://linkedlifedata.com/resource/pubmed/commentcorrection/10477557-9850864
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0022-1007
pubmed:author
pubmed:issnType
Print
pubmed:day
6
pubmed:volume
190
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
733-40
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:10477557-Adoptive Transfer, pubmed-meshheading:10477557-Amino Acid Sequence, pubmed-meshheading:10477557-Animals, pubmed-meshheading:10477557-Antigens, CD, pubmed-meshheading:10477557-Antigens, CD28, pubmed-meshheading:10477557-Antigens, CD80, pubmed-meshheading:10477557-Antigens, CD86, pubmed-meshheading:10477557-Encephalomyelitis, Autoimmune, Experimental, pubmed-meshheading:10477557-Female, pubmed-meshheading:10477557-Lymphocyte Activation, pubmed-meshheading:10477557-Membrane Glycoproteins, pubmed-meshheading:10477557-Mice, pubmed-meshheading:10477557-Mice, Inbred C57BL, pubmed-meshheading:10477557-Mice, Knockout, pubmed-meshheading:10477557-Molecular Sequence Data, pubmed-meshheading:10477557-Myelin Proteins, pubmed-meshheading:10477557-Myelin-Associated Glycoprotein, pubmed-meshheading:10477557-Peptide Fragments, pubmed-meshheading:10477557-T-Lymphocytes, pubmed-meshheading:10477557-Vaccination
pubmed:year
1999
pubmed:articleTitle
Studies in B7-deficient mice reveal a critical role for B7 costimulation in both induction and effector phases of experimental autoimmune encephalomyelitis.
pubmed:affiliation
Immunology Research Division, Department of Pathology, Center for Neurologic Diseases, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't