The Y chromosome from autoimmune BXSB/MpJ mice induces a lupus‐like syndrome in (NZW × C57BL/6)F1 male mice, but not in C57BL/6 male mice
The Y chromosome from autoimmune BXSB/MpJ mice induces a lupus‐like syndrome in (NZW × C57BL/6)F1 male mice, but not in C57BL/6 male mice
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自身免疫 BXSB/MpJ 小鼠的 Y 染色体会在 (NZW × C57BL/6)F1 雄性小鼠中诱导狼疮样综合征，但不会在 C57BL/6 雄性小鼠中诱导狼疮样综合征
DOI：
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发表时间：
1988
影响因子：
5.4
通讯作者：
R. Merino
中科院分区：
文献类型：
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作者：
S. Izui;M. Higaki;D. Morrow;R. Merino
BXSB小鼠的Y染色体已被证明与近交系BXSB小鼠及其与NZB或NZW小鼠杂交的F1狼疮样自身免疫综合征的加速有关。为了进一步确定这种与BXSB Y染色体连锁的未知基因的作用，将Y染色体从BXSB品系转移到非自身免疫的C57BL/6(B6)小鼠中。本文研究了YaA基因在B6小鼠及其与NZW小鼠杂交F1中自身抗体形成和肾小球肾炎发生发展中的作用。BXSB Y染色体的存在不能在B6小鼠中诱导显著的自身免疫反应。然而，携带BXSB Y染色体的(NZW×B6)F1雄性小鼠发生了严重的狼疮样自身免疫综合征，表现为产生抗DNA抗体和gp70-抗gp70免疫复合体，并发展为致死性狼疮性肾炎。无BXSB Y染色体的(NZW×B6)F1两性基本正常。我们的结果表明：(A)BXSB Y染色体本身不足以启动非自身免疫性B6小鼠的自身免疫反应，以及(B)它能够在有可能发展为疾病的小鼠中诱导自身免疫反应，但其常染色体异常本身不足以发展为自身免疫性疾病。
The Y chromosome of the BXSB mouse has been shown to be responsible for the acceleration of lupus‐like autoimmune syndrome in inbred BXSB mice and in their F1 hybrids with NZB or NZW mice. To further define the role of this as yet unidentified gene linked to the BXSB Y chromosome, designated Yaa (Y chromosome‐linked autoimmune acceleration), the Y chromosome was transferred from the BXSB strain to nonautoimmune C57BL/6 (B6) mice. The effect of the Yaa gene on the autoanti‐body formation and the development of glomerulonephritis was investigated in B6 mice and in their F1 hybrids with NZW mice. The presence of the BXSB Y chromosome was not able to induce significant autoimmune responses in B6 mice. However, (NZW × B6)F1 males bearing the BXSB Y chromosome developed a severe lupus‐like autoimmune syndrome, as documented by the production of anti‐DNA antibodies and gp70‐anti‐gp70 immune complexes and the development of lethal lupus nephritis. Both sexes of (NZW × B6)F1 hybrids without the BXSB Y chromosome were essentially normal. Our results suggest that (a) the BXSB Y chromosome by itself is not sufficient to initiate autoimmune responses in nonautoimmune B6 mice, and (b) it is able to induce autoimmune responses in mice potentially capable of developing the disease, but whose autosomal abnormality by itself is not sufficient to develop autoimmune diseases.