Source:http://linkedlifedata.com/resource/pubmed/id/12789294
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
20
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pubmed:dateCreated |
2003-6-5
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pubmed:abstractText |
Cancer cells express self-antigens that are weakly recognized by the immune system. Even though responses against autologous cells are difficult to induce, the immune system is still able to mount a response against cancer. The discovery of the molecular identity of antigens that are recognized by the immune system of melanoma patients has led to the elucidation of tumor immunity at a cellular and molecular level. Multiple pathways in both the priming and effector phases of melanoma rejection have been described. Animal models' active immunotherapies for melanoma show a requirement for the cellular compartment of the immune system in the priming phase, primarily CD4+T cells. More diverse elements are required for the effector phase, including components from the innate immune system (macrophages, complement and/or natural killer cells) and from the adaptive immune system (CD8+T cells and B cells). Minor differences in amino-acid sequences of antigens must determine the particular mechanisms involved in tumor rejection. Since the immune system contains T and B cells that recognize and reject autologous cells, a consequence of tumor immunity is potential autoimmunity. There are distinct pathways for tumor immunity and autoimmunity. The requirements for autoimmunity at the priming phase seem to be CD4+/IFN-gamma dependent while the effector mechanisms are alternative and redundant. Vitiligo (autoimmune hypopigmentation) can be mediated by T cells, FcgammaR+macrophages and/or complement.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0950-9232
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
19
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pubmed:volume |
22
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
3180-7
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:12789294-Animals,
pubmed-meshheading:12789294-Antibodies,
pubmed-meshheading:12789294-Antigens, Differentiation,
pubmed-meshheading:12789294-Antigens, Neoplasm,
pubmed-meshheading:12789294-Autoimmunity,
pubmed-meshheading:12789294-CD8-Positive T-Lymphocytes,
pubmed-meshheading:12789294-Germ Cells,
pubmed-meshheading:12789294-Humans,
pubmed-meshheading:12789294-Immunity, Cellular,
pubmed-meshheading:12789294-Melanoma,
pubmed-meshheading:12789294-Tumor Escape
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pubmed:year |
2003
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pubmed:articleTitle |
Immunity to melanoma: unraveling the relation of tumor immunity and autoimmunity.
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pubmed:affiliation |
Memorial Sloan-Kettering Cancer Center and the Weill Graduate School of Medical Sciences of Cornell University, 1275 York Avenue, New York, NY 10021, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Review,
Research Support, Non-U.S. Gov't
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