Mouse major histocompatibility complex and lung development: haplotype variation, H-2 immunolocalization, and progressive maturation.
Mouse major histocompatibility complex and lung development: haplotype variation, H-2 immunolocalization, and progressive maturation.
复制标题
小鼠主要组织相容性复合体和肺发育:单倍型变异、H-2 免疫定位和渐进成熟。
DOI:
10.1002/ajmg.1320390413
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发表时间:
1991
期刊:
影响因子:
--
通讯作者:
Melnick,M
中科院分区:
文献类型:
--
作者:
Jaskoll,T;Hu,CC;Melnick,M
The association of the mouse major histocom-patibility complex (H-2), lung maturation, and corticosteroid responsiveness has recently been demonstrated in congenic B10 (H-2 b) and B10. A (H-2 a) mice (Hu et al.: American Journal of Medical Genetics 35: 126–131, 1990). We have investigated additional haplotypes [B10. BR (H-2 k) and B10. D2 (H-2 d] to confirm that there is a strong association between H-2 haplotype variation and the degree of pulmonary maturation. Lungs of B10. D2, B10. BR, B10, and B10. A congenic mice achieve haplotypic specific maturation: B10. D2 lungs> B10 lungs= B10. BR lung> B10. A lungs. It appears that the expression of these developmental potentials is under corticosteroid regulation. Further, to test the hypothesis that H-2 antigens would be expressed earlier in embryonic lungs with the H-2 b (BIO) or H-2 k (B10. BR) haplotype than with the H-2 a (B10. A) haplotype, we investigated the spatiotemporal patterns of H-2 antigen localization in B10, B10. BR, and B10. A congenic mouse strains with and without corticostroid treatment. The spatial patterns of H-2 antigen localization was similar in the B10, B10. BR, and B10. A mouse lungs; however, these patterns appeared earlier in both untreated and treated B10 and B10. BR mice as compared with untreated B10. A mice, suggesting an H-2 haplotype associated rate of pulmonary maturation. Following corticosteroid treatment, all congenic strains had a temporally comparable spatial distribution of H-2 antigens. Our results provide preliminary evidence suggesting that both a lung “developmental gene (s)” and a “glucocorticoid responsiveness gene (s)” are most likely outside the KD subregions of the H-2 complex. A model of the H-2 regulation of lung maturation and corticosteroid responsiveness is discussed.