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High MHC class I expression correlates with slow growth in UV‐induced skin carcinomas in hairless mice
Author(s) -
SVANE INGE MARIE,
ENGEL ANNEMARIE,
THOMSEN NIELS BECH,
WULF HANS CHRISTIAN,
WERDELIN OLE
Publication year - 1998
Publication title -
apmis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0903-4641
DOI - 10.1111/j.1699-0463.1998.tb00265.x
Subject(s) - hairless , major histocompatibility complex , mhc class i , biology , cancer research , mhc class ii , cell growth , immunology , pathology , microbiology and biotechnology , immune system , medicine , genetics
An experiment was set up to investigate the relationship, if any, between cell surface MHC class I expression and the growth rate for skin tumors induced by two different UV radiation regimens in hairless mice. Two groups of 20 hairless mice were each irradiated with either a UVA radiation source (2 SED per session) or broad‐spectrum UV radiation (UVB) (8.1 SED per session) 5 days a week during the entire experiment. In the UVA group, 17 out of 20 animals developed tumors, and 10 of these grew to a diameter of ≥5 mm. In the UVB group, 19 out of 20 animals developed tumors, and 15 of these grew to a diameter of ≥5 mm. The tumor induction time, i.e. the time from the start of UV treatment to tumor appearance, was found to be significantly longer (p<0.01) in the UVA than in the UVB group. This is in accordance with previous findings. Of the 25 tumors growing to a diameter of ≥5 mm, 11 were established as cultured cell lines (4 UVA and 7 UVB tumors). These uncloned cell lines were analyzed for surface expression of major histocompatibility complex class I by FACS analysis. There was a clear correlation between high MHC class I expression and slow growth of the individual tumors (p<0.05). This suggests a role for the MHC class I governed, i.e. cytotoxic T‐cell‐mediated, reactions in deciding the fate of UV‐induced skin cancers. No correlation was found between MHC class I expression and tumor induction time.