Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1998-3-18
pubmed:abstractText
Cutaneous painting with reactive haptens induces contact sensitivity (CS) responses that are in vivo examples of T cell immunity. In contrast, high dose i.v. administration of the hapten can induce tolerance. We investigated the effect of IL-12 on reversal of this tolerance and attempted to determine in vitro the mechanism of this reversing effect by measuring proliferation and IFN-gamma production by CS effector T cells stimulated with hapten-conjugated APC, and we also measured CS ear swelling in vivo. The in vitro responses of T cells to hapten-APC became absent in tolerized mice, paralleling impaired in vivo CS responses. Addition of IL-12 to cultures manifesting this fully established in vitro tolerance completely restored impaired responses of tolerized T cells. The reversing effects of IL-12 were not blocked by anti-IFN-gamma mAb, but were blocked by mAbs against B7-1, more strongly by anti-B7-2, and by both Abs together. Additional in vivo ear-swelling response experiments confirmed the reversing effects of IL-12 on established tolerance. To examine whether the IL-12 effect depended on stimulation of IFN-gamma, we directly injected IFN-gamma into tolerized mice. This partially mimicked but did not fully reconstitute the effects of IL-12. In summary, IL-12 abrogation of established tolerance of CS may have been partially due to endogenous production of IFN-gamma, but appeared mainly due to direct activation of the tolerized T cells by affecting signaling through costimulatory molecules B7-1 and B7-2.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
160
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2080-8
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:9498744-Animals, pubmed-meshheading:9498744-Antigens, CD, pubmed-meshheading:9498744-Antigens, CD80, pubmed-meshheading:9498744-Antigens, CD86, pubmed-meshheading:9498744-Cells, Cultured, pubmed-meshheading:9498744-Dermatitis, Contact, pubmed-meshheading:9498744-Edema, pubmed-meshheading:9498744-Epitopes, pubmed-meshheading:9498744-Haptens, pubmed-meshheading:9498744-Immune Tolerance, pubmed-meshheading:9498744-Injections, Intravenous, pubmed-meshheading:9498744-Interferon-gamma, pubmed-meshheading:9498744-Interleukin-12, pubmed-meshheading:9498744-Lymph Nodes, pubmed-meshheading:9498744-Lymphocyte Activation, pubmed-meshheading:9498744-Male, pubmed-meshheading:9498744-Membrane Glycoproteins, pubmed-meshheading:9498744-Mice, pubmed-meshheading:9498744-Mice, Inbred CBA, pubmed-meshheading:9498744-T-Lymphocytes
pubmed:year
1998
pubmed:articleTitle
IL-12 reverses established antigen-specific tolerance of contact sensitivity by affecting costimulatory molecules B7-1 (CD80) and B7-2 (CD86).
pubmed:affiliation
Department of Veterinary Surgery, University of Osaka Prefecture College of Agriculture, Japan.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.