IGG SUBCLASSES IN THE SERUM AND SKIN IN SUBACUTE CUTANEOUS LUPUS-ERYTHEMATOSUS AND NEONATAL LUPUS-ERYTHEMATOSUS

被引:24
作者
BENNION, SD
FERRIS, C
LIEU, TS
REIMER, CB
LEE, LA
机构
[1] DENVER VET ADM HOSP,DENVER,CO
[2] FITZSIMONS ARMY MED CTR,DEPT ELECT ENGN,AURORA,CO 80045
[3] UNIV TEXAS,HLTH SCI CTR,SW MED SCH,DEPT DERMATOL,DALLAS,TX 75235
[4] CTR DIS CONTROL,CTR INFECT DIS,DIV HOST FACTORS,ATLANTA,GA 30333
[5] UNIV COLORADO,SCH MED,DEPT DERMATOL,DENVER,CO 80202
[6] UNIV COLORADO,SCH MED,DEPT MED,DENVER,CO 80202
关键词
D O I
10.1111/1523-1747.ep12514311
中图分类号
R75 [皮肤病学与性病学];
学科分类号
100206 ;
摘要
IgG subclasses differ in their biologic and chemical properties, such as complement fixation, protein and cellular binding, and placental transfer. In this study, IgG subclasses of anti-Ro/SSA antibodies in subacute cutaneous lupus (SCLE) and neonatal lupus (NLE) are examined in the serum and in the skin. IgG subclasses in NLE beginning in utero (NLE-heart disease) are compared to subclasses in NLE beginning after birth (NLE-skin disease). Human skin was grafted onto athymic mice, mice were injected with one of eight anti-Ro/SSA maternal NLE sera (four heart block, four skin disease) or seven anti-Ro/SSA SCLE sera, and grafts were examined for IgG subclasses using monoclonal anti-human IgG subclass reagents in an immunofluorescent technique. Lesional skin was examined from four SCLE patients. IgG1 was the only IgG subclass detected in the grafts and skin lesions. IgG1 was the predominant anti-Ro/SSA IgG subclass detected in SCLE and NLE sera in an ELISA using a synthetic Ro/SSA polypeptide. These studies show that the maternal anti-Ro/SSA autoantibodies in NLE-heart disease sera are predominantly IgG1 and are therefore likely to be present in the fetus at the time of gestation, when heart block usually develops. Second, differences in the clinical presentations of NLE (in utero vs. postnatal disease) cannot be attributed to differences in anti-Ro/SSa IgG subclasses. Finally, the subclass bound in the skin in SCLE is IgG1, a subclass capable of mediating tissue injury via complement or cellular effectors.
引用
收藏
页码:643 / 646
页数:4
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