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Expression of a unique protein on colon cancer cells that reacts with a novel monoclonal antibody and ulcerative colitis serum
Author(s) -
HASSAN T.,
KANISAWA Y.,
MEYERS S.,
DASGUPTA A.,
DAS K. M.
Publication year - 1995
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1995.tb03722.x
Subject(s) - ulcerative colitis , antibody , colorectal cancer , autoantibody , immunology , monoclonal antibody , isotype , medicine , inflammatory bowel disease , immunofluorescence , cancer , in vitro , microbiology and biotechnology , biology , disease , biochemistry
SUMMARY We earlier developed a MoAb, 7E 12 H 12 (IgM isotype), against a protein present in normal colonic epithelial cells. To examine if 7E 12 H 12 ‐reactive protein is expressed in colon cancer cells and is recognized by ulcerative colitis (UC)‐associated autoantibody, we investigated several colon cancer cell lines. 7E 12 H 12 reactivity against the cells was examined by indirect immunofluorescence assay and whole cell ELISA against six colon cancer cell lines HT‐29, LoVo, COLO 205, DLD‐1, LS 180 and SW 1116. A competitive ELISA was developed using 7E 12 H 12 MoAb and patients' serum to examine the cross‐reactive antibodies in the serum. Among the six colon cancer cell lines only LS 180, DLD‐l and SW 1116 reacted with 7E 12 H 12 MoAb, while others did not. The mean (s.e.m.) inhibition of the binding or 7E 12 H 12 MoAb to LS 180 cells by UC serum ( n = 51) was 42±2±1%, whereas in normal subjects ( n = 17) it was 14±2±6%, in Crohn's disease ( n = 19) it was 15±3±2±5%, in infectious diarrhoea ( n = 10) it was 11%±3%, and in systemic lupus erythematosus ( n = 10) it was 2%±0±6%. The inhibition by the UC group was significantly ( P <0±001 ‐ <0±000l) higher than any of the non‐UC groups, and this inhibition was mainly by IgG1 antibody. The protein in the specific colon cancer cells recognized by the 7E 12 H 12 MoAb cross‐reacts with UC‐IgG1 antibody and may provide an in vitro system to examine the autoimmune mechanisms in UC.

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