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Evidence for an immunological attack on the placenta in pemphigoid gestationis
Author(s) -
Borthwick Gillian,
Lawlori Frances,
Holmes R.C.,
Black M.M.,
Stirrat G.M.
Publication year - 1985
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1111/j.1365-2133.1985.tb13009.x
Subject(s) - obstetrics and gynaecology , medicine , university hospital , family medicine , pregnancy , biology , genetics
Pemphigoid gestationis (PG) is characterized immunologically by the deposition of complement (C3) in a linear pattern at the basement membrane zone of skin. It has been proposed that the auto‐antibody responsible may be induced by placental antigens that crossreact with skin (Holmes et al. , 1983). This hypothesis was supported by this study which demonstrated evidence of an immune attack on the placenta in PG. Placental tissue from four patients with PG was examined immunohistologically employing the monoclonal antibodies NFK‐1 which demonstrates HLA‐DR antigen, F10‐89‐4 which recognizes the leukocyte common antigen, and Leu‐M3 which detects a human monocyte‐macrophage antigen. The staining patterns were compared with five normal term placentae. In all of the PG placentae, situated close to the separated decidua within the villi, there were large numbers of Fio‐89‐4‐positive bone marrow derived cells, all of which expressed HLA‐DR antigen. The fetal blood vessels in the villous stroma of one placenta also showed HLA‐DR staining. In the normal placentae, DR antigen was present on only sparse stromal cells and it was absent from fetal blood vessels. Abnormal expression of HLA‐DR antigen has recently been observed on capillary endothelium of thyroid glands in a study of auto‐immune thyroid disease (Hanfusa et al. , 1983) and it has been proposed that aberrant DR expression could be of primary importance in the induction of auto‐immunity. Clinical evidence of an immune attack on the placenta in PG is provided by the increase in frequency of small‐for‐dates infants (Holmes & Black, 1984). The observations presented here indicate that the primary pathological process in PG may be an immune attack on the placenta and the findings also highlight the importance of HLA‐DR antigens in the auto‐immune disease process.