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Concordant Graves' disease after bone marrow transplantation: implications for pathogenesis
F J Holland1, J K McConnon, R Volpé
1Department of Pediatrics, University of Toronto, Ontario, Canada.
The Journal of Clinical Endocrinology and Metabolism
|April 1, 1991
Summary
This study explores Graves' disease pathogenesis, suggesting a male patient acquired autoimmune lymphocytes from his sister via bone marrow transplant. This challenges the traditional view of thyroid-specific antigens triggering the disease.
Area of Science:
- Immunology
- Endocrinology
- Genetics
Background:
- Autoimmune diseases like Graves' disease are thought to arise from gene-environment interactions.
- In Graves' disease, thyroid epithelial cells may express HLA class II antigens, presenting thyroid antigens to lymphocytes.
- Cytokines produced by T-lymphocytes are believed to induce thyrocyte HLA-DR expression.
Observation:
- A sister and brother presented with Graves' disease and ophthalmopathy.
- The brother had previously received a bone marrow transplant from his sister due to aplastic anemia.
- Post-transplant, the brother's leukocytes were genetically identical to his sister's, with complete HLA class I and II antigen identity.
Findings:
- The male patient's Graves' disease developed after receiving his sister's bone marrow.
- Despite no family history or shared HLA-DR3/B8 antigens, both siblings developed Graves' disease.
- The study proposes the male acquired a lymphocyte clone from his sister, causing his hyperthyroidism.
Implications:
- This case suggests that in some instances, Graves' disease may result from acquired, rather than solely endogenous, immune responses.
- The findings challenge the established hypothesis that thyroid-specific antigens are the primary trigger for hyperthyroidism in Graves' disease.
- This highlights the potential role of immune cell transplantation in the development of autoimmune conditions.