Melanoma and innate immunity--aActive inflammation or just erroneous attraction? Melanoma as the source of leukocyte-attracting chemokines.

Details

Serval ID
serval:BIB_8C228BBB0798
Type
Article: article from journal or magazin.
Publication sub-type
Review (review): journal as complete as possible of one specific subject, written based on exhaustive analyses from published work.
Collection
Publications
Title
Melanoma and innate immunity--aActive inflammation or just erroneous attraction? Melanoma as the source of leukocyte-attracting chemokines.
Journal
Seminars in Cancer Biology
Author(s)
Navarini-Meury A.A., Conrad C.
ISSN
1096-3650 (Electronic)
ISSN-L
1044-579X
Publication state
Published
Issued date
2009
Volume
19
Number
2
Pages
84-91
Language
english
Notes
Publication types: Journal Article ; Review
Abstract
Unwanted growth breeds response--in the garden as well as in the tumor microenvironment. Innate immune cells mediate the earliest responses against melanoma or its precursors. However, the actual benefit by those cellular efforts is questionable. Why can early melanoma lesions actually develop in the face of rapid innate responses, and why is neutrophil- and macrophage-attracting chemokine secretion observed in melanoma? A surprisingly similar choice of chemokine receptors and chemokines are present in both innate immune cells and melanoma. Here we focus on analogies and differences between the two. Melanoma cell clusters show active chemokine signalling, with mostly tumor growth-enhancing and leukocyte-attracting effects. However, infiltrating leukocytes have only weak tumoricidal effects. Therefore, the observed leukocyte infiltration in melanoma might be at least in part an epiphenomenon of neoplastic self-stimulation rather than a full-fledged innate anti-tumor immune response.
Keywords
Animals, Chemokines/immunology, Humans, Immunity, Innate, Inflammation/immunology, Leukocytes/immunology, Melanoma/immunology
Pubmed
Web of science
Create date
26/03/2012 10:28
Last modification date
20/08/2019 14:50
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