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FUNCTIONAL STUDIES OF H‐2 k ‐LIKE EPITOPES ON DTIC TREATED AND UNTREATED L1210 (H‐2 d ) CLONES
Author(s) -
Marelli O.E.A.,
Franco P.,
Labeta M.O.,
Festenstein H.
Publication year - 1989
Publication title -
international journal of immunogenetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.41
H-Index - 47
eISSN - 1744-313X
pISSN - 1744-3121
DOI - 10.1111/j.1744-313x.1989.tb00484.x
Subject(s) - in vivo , epitope , in vitro , antigen , monoclonal antibody , cytotoxic t cell , microbiology and biotechnology , clone (java method) , monoclonal , biology , antibody , virology , chemistry , immunology , biochemistry , genetics , dna
SUMMARY Following ‘ in vivo ’ treatment with 5‐(3–3′‐dimethyl‐l‐triazeno)imidazole‐4‐carbox‐amide (DTIC), murine leukemic cells acquire new antigenic specificities not detectable on parental cells and responsible for the rejection of the tumour by syngeneic hosts.‘ In vivo ’ and ‘ in vitro ’ experiments pointed out an immunological cross reactivity between DTIC treated and untreated lines. Furthermore, specific CTLs raised against DTIC treated L1210 tumour cells (H‐2 d ) were cytotoxic for H‐ 2 k target cells. The aim of this study is to investigate whether the H‐2 k cross reactivity displayed by L1210/DTIC is related to the drug treatment rather than due to an antigen already present in the parental line and maintained after treatment. Cloned cells from L1210, obtained by limiting dilution ‘ in vitro ’, were recloned ‘ in vivo ’ and then treated with DTIC. Syngeneic and allogeneic CTLs raised ‘ in vitro ’ against parental and treated clones showed lytic activity against H‐ 2 k target cells. Treated and untreated clones were then checked for the presence of H‐2 k ‐like determinants using monoclonal antibodies. One of these, HB‐53 (IgG2bK k D k was highly positive with all the clones tested in binding assay using iodinated Fab anti‐mouse Ig, fluorescence and FACS analysis. Others displayed a low reactivity against both treated and untreated clones without significant differences. After neuraminidase treatment of two clones (D and D/DTIC), the H‐100.5 (anti H‐2K k )‐reactive epitope was dramatically exposed mi the DTIC tumour cells but not on the parental clones. These data suggest that the H‐2 k cross reactivity is related to the presence of a TAA that is maintained after treatment. Nevertheless DTIC could enhance the expression of some H‐2 k ‐like determinants. So far it is not possible to rule out that this phenomenon can contribute to increase the antigenicity of DTIC clones.