Immune reconstitution syndrome and the thyroid
Abstract
Reconstitution Graves' disease occurs in three settings. First, bone marrow transplantation from a donor with Graves' disease may cause this disease to appear in the recipient, as a result of adoptive immunity, although disordered immunoregulation secondary to graft-versus-host disease may also play a role. Second, alemtuzumab treatment for multiple sclerosis leads to the development of Graves' disease in up to a third of patients during the phase of naive T-cell expansion, which follows therapeutic lymphocyte depletion. Other reconstitution autoimmune phenomena, including immune thrombocytopaenic purpura, are also recognised after alemtuzumab administration. Finally, reconstitution Graves' disease may occur during a similar phase of CD4(+) T-cell expansion, which follows highly active antiretroviral therapy for human immunodeficiency virus infection. Again, this complication is part of a broader spectrum of immunoregulatory disturbances, which can arise after immune reconstitution. The mechanisms responsible for reconstitution Graves' disease are at present unclear, but may include a relative bias towards a Th2-mediated immune response and reduced competition for autoreactive lymphocytes to expand during the time when recovery from lymphopenia commences.
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Secondary autoimmunity following allogeneic BMT/HSCT arises by additional mechanisms distinguishing it from other IRTs, including adoptive immunity and graft-versus-host disease with loss of regulation of autoreactive T lymphocytes.
“Secondary autoimmunity following allogeneic BMT/HSCT arises by additional mechanisms distinguishing it from the other IRTs including: (1) adoptive immunity, that is transferral of autoreactive lymphocyte clones from the donor to the recipient and (2) graft-versus-host disease with the loss of regulation of autoreactive T lymphocytes previously kept under control by peripheral immune tolerance [11,”
From 2019 European Thyroid Association Guidelines on the Management of Thyroid Dysfunction following Immune Reconstitution Therapy (2019) · cites this paper as [11]
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- Authors
- Weetman, A.
- Affiliations
- University of Sheffield (GB)
- Corresponding author
- Weetman, Anthony
- ORCID
- Weetman, Anthony
- Venue
- Best Practice & Research Clinical Endocrinology & Metabolism
- Publisher
- Elsevier BV
- Published
- 2009-12
- Volume
- 23
- Issue
- 6
- Pages
- 693-702
- ISSN
- 1521-690X (ISSN-L)
- OpenAlex
- W2085833314
- Cited by
- 87
- References
- 58
- Citations by year
- 2025: 1 · 2024: 5 · 2023: 4 · 2022: 3 · 2021: 4 · 2020: 4 · 2019: 3 · 2018: 5 · 2017: 4 · 2016: 4 · 2015: 7 · 2014: 13 · 2013: 11 · 2012: 9
- FWCI
- 0.83
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Best Practice & Research Clinical Endocrinology & Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Disorders and Treatments
- Life Sciences › Immunology and Microbiology › Immunology › Immunodeficiency and Autoimmune Disorders
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Keywords
- immune reconstitution inflammatory syndrome, Graves' disease, bone marrow transplantation, alemtuzumab, multiple sclerosis, lymphocyte depletion, antiretroviral therapy, HIV infection, CD4+ T cell expansion, lymphopenia, Th2 immune response, graft-versus-host disease, autoimmune thyroid disease
- MeSH terms
- Alemtuzumab, Antibodies, Monoclonal, Antibodies, Neoplasm, Autoimmune Diseases, Graft vs Host Disease, Graves Disease, Humans, Multiple Sclerosis, Thyroid Gland, Bone Marrow Transplantation, Antiretroviral Therapy, Highly Active, Immune Reconstitution Inflammatory Syndrome, Antibodies, Monoclonal, Humanized
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