Linked Life Data

2428509

Source:http://linkedlifedata.com/resource/pubmed/id/2428509

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1986-10-31
pubmed:abstractText
Two monoclonal antibodies, OX-6 and OX-17, were used to evaluate respectively the roles of I-A and I-E major histocompatibility complex Class II gene products in the in vitro activation and subsequent function in recipient rats of encephalitogenic T-cell lines. Activation of the T-cell lines with guinea pig myelin basic protein (GP-BP) presented by accessory cells (APC) resulted in an increase in the number of blast cells in culture and was reflected by increased uptake of [3H]thymidine [( 3H]Tdy). The number of blasts recovered and [3H]Tdy uptake during activation was reduced drastically in the presence of OX-6, but to a much lesser extent in the presence of OX-17. OX-6 but not OX-17 appeared to block T-cell activation primarily by inhibiting APC function, since preincubation of APC but not T cells with OX-6 before stimulation resulted in complete inhibition of the cultures. After activation, the BP-1 T-cell line or D-9 clone transferred severe paralysis to normal recipient rats. Recipients of OX-6-treated BP-1 or D-9 T cells exhibited very mild or no signs, whereas recipients of OX-17-treated cells developed only slightly less severe experimental autoimmune encephalomyelitis (EAE) than recipients of untreated encephalitogenic control cultures. In contrast, treatment with OX-17 but not OX-6 reduced the ability of BP-reactive T cells to transfer delayed-type hypersensitivity reactions. Dermal testing with GP-BP in the ears of recipient rats just prior to onset of clinical signs decreased significantly the clinical intensity of EAE induced by activated BP-reactive T cells, but increased the clinical scores in rats which received unstimulated or OX-6-treated T cells. This potentiating effect of GP-BP was due most likely to the presentation of processed antigen to circulating BP-reactive T cells by APC in the ear. These results suggest that both the I-A and I-E gene products may contribute to the activation and subsequent function of encephalitogenic T cells, perhaps through separate mechanisms.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0008-8749
pubmed:author
pubmed:issnType
Print
pubmed:volume
100
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
364-73
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1986
pubmed:articleTitle
Antibodies against I-A and I-E determinants inhibit the activation and function of encephalitogenic T-lymphocyte lines.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't