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Antibody-induced loss of Friend virus leukemia cell surface antigens occurs during progression of erythroleukemia in F1 mice
| Content Provider | Semantic Scholar |
|---|---|
| Author | Doig, D. Chesebro, Bruce |
| Copyright Year | 1978 |
| Abstract | Friend virus (FV)-induced leukemic spleen cells from (B10.A X A)F1 mice were found to lose sensitivity to antibody-mediated lysis during progression of erythroleukemia. This was correlated with a 78% loss of FV-induced cell surface antigens as determined by quantitative absorption of cytotoxic antibodies and with a decreased percentage of leukemic spleen cells showing membrane immunofluorescence with anti-FV antibody. Antigen loss was observed only with virus-induced antigens, and was limited to antigens expressed on the cell surface. FV-induced antigens were regained when low-antigen leukemia cells from late stages of the leukemia were transferred to lethally irradiated nonimmune recipients, but not when these cells were transferred to hyperimmune lethally irradiated recipients. Conversely, when high-antigen leukemic spleen cells from early stages of the erythroleukemia were transferred to hyperimmune irradiated recipients, antigen loss was induced. The immune response to virus-induced antigens appeared to be involved in causing the antigenic changes observed on leukemia cells in this system. |
| Starting Page | 1109 |
| Ending Page | 1121 |
| Page Count | 13 |
| File Format | PDF HTM / HTML |
| PubMed reference number | 281446v1 |
| Volume Number | 148 |
| Journal | The Journal of experimental medicine |
| Alternate Webpage(s) | http://ftp.ncbi.nlm.nih.gov/pub/pmc/d3/73/je14851109.PMC2185041.pdf |
| Language | English |
| Access Restriction | Open |
| Subject Keyword | Acute Erythroblastic Leukemia Antigens, Heterophile Antiviral Response Fluorescent Antibody Technique Friend Murine Leukemia Virus HIV Antigens Leukemia, B-Cell Murine sarcoma viruses Therapeutic radiology procedure Tissue membrane hearing impairment pathologic cytolysis |
| Content Type | Text |
| Resource Type | Article |