Potentiation of therapeutic effect of recombinant tumour necrosis factor against B16 mouse melanoma by combination with recombinant interleukin 2
Cytokine, ISSN: 1043-4666, Vol: 5, Issue: 3, Page: 224-229
1993
- 4Citations
- 2Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations4
- Citation Indexes4
- CrossRef3
- Captures2
- Readers2
Article Description
Treatment of B16 melanoma-bearing mice with recombinant tumour necrosis factor (rTNF) caused a marked inhibition of tumour growth but did not result in the complete cure of the tumour-bearing mice. In contrast, combination therapy of B16-bearing mice with r-TNF and recombinant interleukin 2 (rIL-2) potentiated the therapeutic effect of rTNF and 30% of the mice were totally cured from tumour. Spleen cells obtained from B16-bearing mice showed markedly decreased immune responses including IL-2 production, IL-2 responsiveness and mixed lymphocyte reaction owing to the existence of suppressor macrophages. However, spleen cells obtained from mice cured with rTNF plus rIL-2 showed the same level of T cell responsiveness as that from normal mice. The decreased induction of alloantigen-specific cytotoxic T lymphocytes (CTL) in B16-bearing mice was also recovered after treatment with rTNF plus rIL-2. Moreover, B16-specific CTL, which could not be induced in normal or B16-bearing mice, was effectively induced from the spleen cells of B16-cured mice by rTNF and rIL-2. These results demonstrated that local therapy of melanoma with rTNF and rIL-2 was effective and induced systemic antitumour immunity in vivo.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/104346669390008S; http://dx.doi.org/10.1016/1043-4666(93)90008-s; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0027443301&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/8218934; http://linkinghub.elsevier.com/retrieve/pii/104346669390008S; http://api.elsevier.com/content/article/PII:104346669390008S?httpAccept=text/xml; http://api.elsevier.com/content/article/PII:104346669390008S?httpAccept=text/plain; https://linkinghub.elsevier.com/retrieve/pii/104346669390008S; http://dx.doi.org/10.1016/1043-4666%2893%2990008-s; https://dx.doi.org/10.1016/1043-4666%2893%2990008-s
Elsevier BV
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