August 13, 2021
Keio University School of Medicine
A research group led by Professor Masayuki Amagai and Collaborative Researcher Shohei Eto of the Department of Dermatology, Keio University School of Medicine, and Associate Professor Jun Yamagami of Tokyo Women's Medical University (who was a Senior Lecturer at the Department of Dermatology, Keio University School of Medicine at the time of the research) has discovered that in neonatal linear IgA bullous dermatosis, the IgA antibodies that cause the disease are present in the mother's breast milk.
Neonatal linear IgA bullous dermatosis is a rare disease that causes blisters and erosions via IgA antibodies that bind to the junction between the epidermis and dermis (the dermoepidermal junction). Lesions are often seen not only on the skin but also in the mucosal airways, leading to a life-threatening condition. While many neonatal autoimmune skin diseases are caused by pathogenic antibodies (autoantibodies) in the mother's blood being transferred to the fetus through the placenta, in linear IgA bullous dermatosis, previous reports have not found pathogenic antibodies in the mother's blood, and their origin was unknown.
In this study, the group demonstrated the presence of IgA antibodies that bind to the dermoepidermal junction in the breast milk of the mother of the affected newborn. They also found that the IgA antibodies deposited on the patient's skin were of the secretory type found in breast milk, not the serum type found in the blood, proving that the IgA antibodies were transferred to the infant via breast milk.
This suggests that in cases of neonatal IgA bullous dermatosis, promptly discontinuing breastfeeding can prevent the condition from becoming severe and can be life-saving.
These research findings were published in the online early-release version of the American scientific journal "JAMA Dermatology" on July 14, 2021 (US Central Standard Time).
Please see below for the full press release.