Antibody‐Binding to the 180‐kD Bullous Pemphigoid Antigens at the Lateral Cell Surface Causes Their Internalization and Inhibits Their Assembly at the Basal Cell Surface in Cultured Keratinocytes
Antibody‐Binding to the 180‐kD Bullous Pemphigoid Antigens at the Lateral Cell Surface Causes Their Internalization and Inhibits Their Assembly at the Basal Cell Surface in Cultured Keratinocytes
复制标题
在培养的角质形成细胞中,抗体与外侧细胞表面的 180-kD 大疱性类天疱疮抗原结合导致其内化并抑制其在基底细胞表面的组装
DOI:
10.1111/j.1346-8138.1994.tb03299.x
复制
发表时间:
1994
期刊:
影响因子:
--
通讯作者:
H. Yaoita
中科院分区:
文献类型:
--
作者:
Y. Kitajima;Y. Hirako;K. Owaribe;S. Mori;H. Yaoita
We demonstrated the effects of monoclonal antibodies to the 180‐kD and 230‐kD BP antigens (BPA) and of BP sera on Ca++‐induced formation of hemidesmosomes in cultured human keratinocytes (a cell line, DJM‐1) by immunofluorescence microscopy. Under low Ca++ (0.07 mM) conditions, the 180‐kD and 230‐kD BPAs were distributed homogeneously on the basal plasma membrane, while they formed a peculiar concentric ring or arch (ring/arch) arrangement in high‐Ca++ (1.87 mM) medium. On the other hand, the apical‐lateral cell membrane was stained homogeneously with antibodies to the 180‐kD BPA, but not to the 230‐kD BPA, both in low and high Ca++ media. The low‐high Ca++ switch at first caused disappearance of the antigen from the basal plasma membrane and then formed the high‐Ca++ ring/arch pattern within 3 hrs. In this system, monoclonal antibodies to the 180‐kD and 230‐kD BPAs and the sera from 5 BP patients, 2 pemphigus vulgaris (PV) patients, and 4 normal volunteers were added into the culture media. The addition of anti‐180‐kD BPA antibodies or any BP serum caused the internalization of the 180‐kD BPA from the apical‐lateral cell membrane and inhibited the Ca++‐induced formation of the ring/arch pattern on the basal membrane, possibly by inhibiting the movement of the antigen from the lateral to the basal membrane to form hemidesmosomes. The internalized fluorescence dots were shown to be composed of the 180‐kD BPA and patient's IgG, but not of the 230‐kD BPA by double‐immunostaining, suggesting the internalized 180‐kD BPA was from the apical‐lateral membrane, but not from hemidesmosomes. Monoclonal antibodies to the 230‐kD BPA and normal and PV sera did not cause these effects. These results suggest that autoantibodies to the 180‐kD BPA, but not to the 230‐kD BPA, may directly bind the antigen on the cell surface and disturb the formation of hemidesmosomes.
登录
查看更多内容
DOI:
10.1016/s0141-8130(05)80004-2
发表时间:
1992-06-01
影响因子:
8.2
作者:
GREEN, KJ;VIRATA, MLA;PARRY, DAD
通讯作者:
PARRY, DAD
DOI:
--
发表时间:
1991
期刊:
The Journal of biological chemistry
影响因子:
--
作者:
Sawamura,D;Li,K;Chu,ML;Uitto,J
通讯作者:
Uitto,J
DOI:
10.1111/1523-1747.ep12876194
发表时间:
1990
期刊:
The Journal of investigative dermatology
影响因子:
--
作者:
Meyer,LJ;Taylor,TB;Kadunce,DP;Zone,JJ
通讯作者:
Zone,JJ
影响因子:
4.4
作者:
Ramzy S. Labib;G. Anhalt;Harikrishna Patel;D. Mutasim;L. Diaz
通讯作者:
Ramzy S. Labib;G. Anhalt;Harikrishna Patel;D. Mutasim;L. Diaz
DOI:
10.1111/1523-1747.ep12276893
发表时间:
1985
期刊:
The Journal of investigative dermatology
影响因子:
--
作者:
Takahashi,Y;Mutasim,DF;Patel,HP;Anhalt,GJ;Labib,RS;Diaz,LA
通讯作者:
Diaz,LA