ArticleClinical and experimental immunology2005
Interactions between the mannose receptor and thyroid autoantigens.
Article in Clinical and experimental immunology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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The trial behind it
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Who cites it
14 citing papers in PubMed, 28 citations in OpenAlex.
- Beyond Sequence: Posttranslational Remodeling of Antigens in Autoimmunity.Immunological reviews · 2026Review
- Monoclonal Antibodies to Thyrotropin Receptor With Thyroid-Stimulating Activity Activate the NF-κB Pathway to Induce Chemokine Expression.Journal of cellular and molecular medicine · 2025Article
- Glycosylation in Autoimmune Diseases.Advances in experimental medicine and biology · 2021Article
- Antibody-Based Tracers for PET/SPECT Imaging of Chronic Inflammatory Diseases.Chembiochem : a European journal of chemical biology · 2019Review
- Molecular Insights Into the Relationship Between Autoimmune Thyroid Diseases and Breast Cancer: A Critical Perspective on Autoimmunity and ER Stress.Frontiers in immunology · 2019Review
- Glycosylation in the Thyroid Gland: Vital Aspects of Glycoprotein Function in Thyrocyte Physiology and Thyroid Disorders.International journal of molecular sciences · 2018Review
- TSH Receptor Cleavage Into Subunits and Shedding of the A-Subunit; A Molecular and Clinical Perspective.Endocrine reviews · 2016Review
- Withdrawn: TSH Receptor Cleavage Into Subunits and Shedding of the A-Subunit; A Molecular and Clinical Perspective.Endocrine reviews · 2016Review
- Breaking tolerance to thyroid antigens: changing concepts in thyroid autoimmunity.Endocrine reviews · 2014Review
- Review and hypothesis: does Graves' disease develop in non-human great apes?Thyroid : official journal of the American Thyroid Association · 2011Review
- An attempt to induce "Graves' disease of the gonads" by immunizing mice with the luteinizing hormone receptor provides insight into breaking tolerance to self-antigens.Thyroid : official journal of the American Thyroid Association · 2011Article
- Anti-Saccaromyces Cerevisiae antibodies (ASCA) are elevated in autoimmune thyroid disease ASCA in autoimmune thyroid disease.Endocrine · 2010Article
- Attenuation of induced hyperthyroidism in mice by pretreatment with thyrotropin receptor protein: deviation of thyroid-stimulating to nonfunctional antibodies.Endocrinology · 2009Article
- A role for exposed mannosylations in presentation of human therapeutic self-proteins to CD4+ T lymphocytes.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Thyroid autoantigens require internalization and processing by antigen-presenting cells to induce immune responses. Besides pinocytosis, antigen uptake can be receptor-mediated. The mannose receptor (ManR) has a cysteine rich domain (CR) and eight carbohydrate recognition domains (CRD) that bind glycosylated proteins. The TSH receptor (TSHR), thyroid peroxidase (TPO) and thyroglobulin (Tg) are glycoproteins. To investigate a role for the ManR in thyroid autoimmunity, we tested the interaction between these autoantigens and chimeric ManRs. Plasmids encoding the CR-domain linked to IgG-Fc (CR-Fc) and CDR domains 4-7 linked to IgG-Fc (CDR4-7-Fc) were expressed and purified with Protein A. Enzyme-linked immunosorbent assay (ELISA) plates were coated with human thyroid autoantigens and CR-Fc or CRD4-7-Fc binding detected with peroxidase-conjugated anti-IgG-Fc. CRD4-7-Fc binding was highest for the TSHR, followed by Tg and was minimal for TPO. CR-Fc bound to Tg but not to TSHR or TPO. The interaction between the TSHR and CRD-Fc was calcium-dependent; it was inhibited by mannose (not galactose), and required a glycosylated TSHR A-subunit. Moreover, precomplexing the TSHR A-subunit with CRD-Fc (but not CR-Fc), or adding mannose (but not galactose), decreased in vitro responses of splenocytes from TSHR-immunized mice. Our data indicate that the ManR may participate in autoimmune responses to Tg and the TSHR but not to TPO. Most important, ManR binding of heavily glycosylated TSHR A-subunits suggests a mechanism by which the minute amounts of A-subunit protein shed from the thyroid may be captured by antigen-presenting cells located in the gland or in draining lymph nodes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.