| Autor: |
Panoskaltsis‐Mortari, Angela, Egeler, R. Maarten, Yaeger, Thomas M., Yoneji, Sumiko, Schmitz, Laura, Lilly, Frank, Nesbit, Mark E., Blazar, Bruce R. |
| Zdroj: |
Journal of Leukocyte Biology; October 1998, Vol. 64 Issue: 4 p441-450, 10p |
| Abstrakt: |
Malignant histiocytosis sarcoma virus (MHSV) arose as a recombinant of c‐Harvey‐ras murine sarcoma virus (Ha‐MuSV) and Friend mink cell focus‐forming virus (F‐MCFV). It is a defective acute transforming retrovirus that, along with Friend murine leukemia helper virus (F‐MuLV), induces malignant histiocytosis (MH) in susceptible adult mice. We have assessed the in vivosusceptibility to MHSV in inbred homozygous, F1 hybrid, congenic, and recombinant inbred (RI) mice. We have shown that: (1) in vivoresistance to MHSV is multigenic, regulated by MHC and non‐MHC genes in a different fashion than with F‐MCFV, F‐MuLV, or Ha‐MuSV; (2) using BXD RI mice, the resistance phenotype is linked with 95.8% probability to two linked loci, Pmv‐9and Iapls3‐14, on chromosome 13 (homologous to the area of human chromosome 5 for which a chromosomal break point at position 5q35 is associated with human MH); and (3) CD4+T cells are critical for MHSV resistance. J. Leukoc. Biol. 64: 441–450; 1998. |
| Databáze: |
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