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Susceptibility of H-2 and Ly Congenic Mice to Ehrlich Ascites Tumors

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It has been shown that mice such as AKR/J (H-2^k), C3H/He (H-2^k), CBA/J (H-2^k), DBA/1 (H-2^q) and DBA/2 (H-2^d) are susceptible to Ehrlich ascites tumor (EAT), while other mice such as A/J (H-2^a), BALB/c (H-2^d), C57BL/6(H-2^b), C57BL/10(H-2^b), NZB/N(H-2^d) and SJL (H-2^s) are resistant to EAT. In addition, Ly haplotypes of the former EAT-progressive mouse strains classified were Ly-1^a (except AKR) and Ly-2^a, and those of the latter EAT-regressive mouse strains displayed Ly-1^b and Ly-2^b as common features. To see how the shift restricted in H-2 or in Ly haplotype affects their susceptibility, EAT progression in H-2 congenic and in Ly congenic mice was compared with that in standard mice. The results are as follows. 1) B10(H-2^b) as a standard was EAT-regressive. B10. D2(H-2^d), which is H-2 congenic between B10(H-2^b) and DBA/2(H-2^d), was EAT-regressive, although the H-2 locus of B10 shifted to the haplotype d of DBA/2. DBA/2 itself is EAT-progressive. This indicates that at least H-2K and/or D loci as class I are not simply related to mouse strain susceptibility to EAT. B10.Y (H-2^<pa>) was EAT-regressive. B10.R III (H-2^r) was almost EAT-regressive with some individual variations. B10.BR (H-2^k) and B10.SM (H-2^v) were EAT-progressive. In short, a shift in H-2 haplotype from b to k or b to v is significant in changing B10 susceptibility to EAT. 2) B6(H-2^b, Ly-1^b, Ly-2^b) as a standard was EAT-regressive. B6-Ly-1^a (H-2^b, Ly-1^a, Ly-2^b), B6-Ly-2^a (H-2^b, Ly-1^b, Ly-2^a) and B6-Ly-2^a, 3^a (H-2^b, Ly-1^b, Ly-2^a, Ly-3^a) were all EAT-regressive. No change in susceptibility was produced by the Ly-1,2,3,haplotype shift. Other B6 congenic mice such as B6-Tla^a (H-2K^k・D^b) and B6.C-H-2^<bm12>(H-2Aβ : bm12) were also EAT-regressive. From the results, it is concluded that H-2K, D loci including the TL region as class I, I-Aβ subregion as class II or Ly-1,2,3 loci, are not simply related to mouse strain susceptibility to EAT, suggesting the participation of non-MHC genes under H-2 associated control.

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