| http://purl.uniprot.org/citations/9570526 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/9570526 | http://www.w3.org/2000/01/rdf-schema#comment | "IL-12p70, a 70-to 75-kDa heterodimer consisting of disulfide-bonded 35-kDa (p35) and 40-kDa (p40) subunits, enhances Th1 development primarily by its ability to induce IFN-gamma production by NK and Th1 cells. Although homodimers of the p40 subunit of IL-12 are potent IL-12 receptor antagonists in some systems, we have reported that p40 homodimer may accentuate alloreactive CD8+ Th1 function. To test the role of endogenously produced p40 in alloimmunity, Th1 development was assessed in either IL-12 p35 knockout (p35-/-) mice, the cells of which are capable of secreting p40, or p40 knockout (p40-/-) mice. Compared with IL-12 wild-type controls, splenocytes obtained from both p35-/- and p40-/-mice produced markedly less IFN-gamma after in vitro stimulation with Con A or alloantigens. Interestingly, in vivo-sensitized Th1 were detected in both p35-/- and p40-/-cardiac allograft recipients. However, in vivo Th1 development was enhanced in p35-/- recipients compared with p40-/-animals, suggesting that endogenous p40 produced in p35-/-mice may stimulate alloreactive Th1. Indeed, neutralizing endogenous p40 with anti-IL-12 p40 mAb reduced Th1 development in p35-/-allograft recipients to that seen in p40-/-mice. To determine whether Th1 development that occurred in the absence of IL-12p70 and p40 required IFN-gamma, p40-/-allograft recipients were treated with anti-IFN-gamma mAb. Neutralizing IFN-gamma did not inhibit in vivo Th1 development in p40-/-recipients and resulted in a unique pathology of rejection characterized by vascular thromboses. Collectively, these data suggest that 1) endogenous p40 may substitute for IL-12p70 in alloantigen-specific Th1 sensitization in vivo and 2) in vivo alloreactive Th1 development may occur independent of IL-12 and IFN-gamma, suggesting an alternate Th1-sensitizing pathway."xsd:string |
| http://purl.uniprot.org/citations/9570526 | http://purl.uniprot.org/core/author | "Li K."xsd:string |
| http://purl.uniprot.org/citations/9570526 | http://purl.uniprot.org/core/author | "Chan S.Y."xsd:string |
| http://purl.uniprot.org/citations/9570526 | http://purl.uniprot.org/core/author | "Bishop D.K."xsd:string |
| http://purl.uniprot.org/citations/9570526 | http://purl.uniprot.org/core/author | "Magram J."xsd:string |
| http://purl.uniprot.org/citations/9570526 | http://purl.uniprot.org/core/author | "Ferrante J."xsd:string |
| http://purl.uniprot.org/citations/9570526 | http://purl.uniprot.org/core/author | "Eichwald E.J."xsd:string |
| http://purl.uniprot.org/citations/9570526 | http://purl.uniprot.org/core/author | "Piccotti J.R."xsd:string |
| http://purl.uniprot.org/citations/9570526 | http://purl.uniprot.org/core/date | "1998"xsd:gYear |
| http://purl.uniprot.org/citations/9570526 | http://purl.uniprot.org/core/name | "J Immunol"xsd:string |
| http://purl.uniprot.org/citations/9570526 | http://purl.uniprot.org/core/pages | "1132-1138"xsd:string |
| http://purl.uniprot.org/citations/9570526 | http://purl.uniprot.org/core/title | "Alloantigen-reactive Th1 development in IL-12-deficient mice."xsd:string |
| http://purl.uniprot.org/citations/9570526 | http://purl.uniprot.org/core/volume | "160"xsd:string |
| http://purl.uniprot.org/citations/9570526 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/9570526 |
| http://purl.uniprot.org/citations/9570526 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/9570526 |
| http://purl.uniprot.org/uniprot/#_F8WI71-mappedCitation-9570526 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/9570526 |
| http://purl.uniprot.org/uniprot/#_Q3ZAX5-mappedCitation-9570526 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/9570526 |
| http://purl.uniprot.org/uniprot/#_P43431-mappedCitation-9570526 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/9570526 |
| http://purl.uniprot.org/uniprot/#_P43432-mappedCitation-9570526 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/9570526 |
| http://purl.uniprot.org/uniprot/#_Q549G3-mappedCitation-9570526 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/9570526 |
| http://purl.uniprot.org/uniprot/#_Q9QUT1-mappedCitation-9570526 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/9570526 |
| http://purl.uniprot.org/uniprot/P43431 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/9570526 |
| http://purl.uniprot.org/uniprot/Q549G3 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/9570526 |
| http://purl.uniprot.org/uniprot/P43432 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/9570526 |