Induction of experimental autoimmune sialoadenitis by immunization of PL/J mice with carbonic anhydrase II.

Induction of experimental autoimmune sialoadenitis by immunization of PL/J mice with carbonic anhydrase II.
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DOI:
10.4049/jimmunol.154.9.4865
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发表时间:
1995-05
影响因子:
4.4
通讯作者:
I. Nishimori;T. Bratanova;I. Toshkov;T. Caffrey;M. Mogaki;Y. Shibata;Michael A. Hollingsworth
I. Nishimori;T. Bratanova;I. Toshkov;T. Caffrey;M. Mogaki;Y. Shibata;Michael A. Hollingsworth
中科院分区:
医学2区
文献类型:
--
作者:
I. Nishimori;T. Bratanova;I. Toshkov;T. Caffrey;M. Mogaki;Y. Shibata;Michael A. Hollingsworth

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用人碳酸酐酶Ⅱ(CAII)和含单磷酰脂质A和海藻糖二氨基真菌酸酯的佐剂皮内免疫PL/J(H-2u)小鼠,诱导实验性自身免疫性涎腺炎。与仅用佐剂免疫的小鼠和未处理的小鼠相比,用CAII免疫的小鼠显示出唾液腺中淋巴细胞浸润的病灶的数量和大小的显著增加。在用CAII免疫的小鼠中,在唾液腺中的闰管和小叶内导管周围观察到淋巴细胞灶,导致腺泡单位萎缩和替换。邻近淋巴细胞灶的涎腺导管上皮细胞既有退行性改变,又有再生性改变。在用CAII免疫的少数小鼠的胰腺和肾脏中观察到类似的淋巴细胞浸润。在具有不同H-2单倍型(p、q、r、s和u)的几个小鼠品系中,具有H-2s和H-2u的品系对CAII诱导的涎腺炎敏感。这些结果表明,在小鼠中由CAII免疫诱导的涎腺炎可以作为干燥综合征的疾病模型,并且与MHC相关的CAII或其衍生肽可能是该综合征中由自身免疫应答识别的一种Ag。
Experimental autoimmune sialoadenitis was induced in PL/J (H-2u) mice by intradermal immunization with human carbonic anhydrase II (CAII) and adjuvant containing monophosphoryl lipid A and trehalose diorynomycolate. Mice immunized with CAII showed a significant increase in the number and size of foci with lymphocytic infiltration in the salivary gland compared with mice immunized with adjuvant alone and untreated mice. In mice immunized with CAII, lymphocytic foci were observed around intercalated and intralobular ducts in the salivary glands, resulting in atrophy and replacement of acinar units. The epithelial cells of salivary ducts adjacent to the lymphocytic foci showed both degenerative and regenerative changes. Similar lymphocytic infiltrations were observed in the pancreas and kidney of a few mice immunized with CAII. Among several mouse strains with different H-2 haplotypes (p, q, r, s, and u), strains bearing H-2s and H-2u were susceptible to CAII-induced sialoadenitis. These results indicate that sialoadenitis induced by the immunization of CAII in mice may serve as a disease model of Sjögren's syndrome and that CAII or its derived peptides in association with the MHC may be one Ag recognized by an autoimmune response in this syndrome.