Chemically induced sarcomas from nude mice are more immunogenic than similar sarcomas from congenic normal mice

IM Svane, AM Engel, MB Nielsen… - European journal of …, 1996 - Wiley Online Library
IM Svane, AM Engel, MB Nielsen, HG Ljunggren, J Rygaard, O Werdelin
European journal of immunology, 1996Wiley Online Library
To detect possible differences in immunogenicity between tumors induced in T cell‐deficient
mice and phenotypically normal congenic mice, 16 sarcomas, 8 having developed in nude
BALB/c mice and 8 having developed in congenic normal (nu/+) mice, were transplanted to
normal BALB/c recipients and the rates of rejection or acceptance were registered. The 16
tumors were chosen randomly from a panel of 39 sarcomas induced with 0.5% or 0.1% 3‐
methylcholanthrene and maintained as cell lines in culture. Out of the tumors originating …
Abstract
To detect possible differences in immunogenicity between tumors induced in T cell‐deficient mice and phenotypically normal congenic mice, 16 sarcomas, 8 having developed in nude BALB/c mice and 8 having developed in congenic normal (nu/+) mice, were transplanted to normal BALB/c recipients and the rates of rejection or acceptance were registered. The 16 tumors were chosen randomly from a panel of 39 sarcomas induced with 0.5% or 0.1% 3‐methylcholanthrene and maintained as cell lines in culture. Out of the tumors originating from nude mice, 66% were rejected by the normal BALB/c recipients, while only 30% of the tumors originating from normal mice were rejected. Tumors with short induction times from normal mice were more readily accepted than tumors with long induction times. Tumors originating from nude mice had significantly longer mean latency times after transplantation to both normal and nude recipients than tumors originating from normal mice. Contrary to what has been reported by others, there was no correlation between the rejection rates of the individual tumors and their Kd, Dd or Ld major histocompatibility complex (MHC) class I surface expression as measured by flow cytometric analysis of cultured tumor cells. The Kd, Dd and Ld proteins of the transplanted tumor lines were analyzed by isoelectric focusing for the occurrence of mutations resulting in altered charge of the MHC protein. No such mutations were found, ruling out MHC mutations of that kind as the source of immunogenicity in the cell lines used in these experiments. Our results suggest the existence of a T cell‐mediated selection in the original tumor cell mass of tumors induced in normal mice, adapting the tumor to growth in a host with a functional T cell system, but apparently there is no connection between this loss of immunogenicity and loss of MHC class I expression.
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