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Related Experiment Videos

Interactions between the mannose receptor and thyroid autoantigens.

G D Chazenbalk1, P N Pichurin, J Guo

  • 1Autoimmune Disease Unit, Cedars-Sinai Research Institute and UCLA School of Medicine, Los Angeles, CA 90048, USA.

Clinical and Experimental Immunology
|January 19, 2005
PubMed
Summary

The mannose receptor (ManR) may contribute to thyroid autoimmunity by binding to thyroid autoantigens like the TSH receptor and thyroglobulin. This interaction suggests a mechanism for antigen uptake by immune cells in thyroid disease.

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Area of Science:

  • Immunology
  • Endocrinology
  • Molecular Biology

Background:

  • Thyroid autoantigens must be internalized and processed by antigen-presenting cells to trigger immune responses.
  • Receptor-mediated uptake is a key mechanism for antigen presentation, alongside pinocytosis.
  • The mannose receptor (ManR) recognizes glycosylated proteins via its carbohydrate recognition domains (CRDs).

Purpose of the Study:

  • To investigate the potential role of the mannose receptor (ManR) in thyroid autoimmunity.
  • To examine the interaction between ManR and key thyroid autoantigens: TSH receptor (TSHR), thyroid peroxidase (TPO), and thyroglobulin (Tg).

Main Methods:

  • Expression and purification of chimeric ManR constructs (CR-Fc and CRD4-7-Fc).
  • Enzyme-linked immunosorbent assay (ELISA) to detect binding of chimeric ManRs to immobilized thyroid autoantigens.

Related Experiment Videos

  • Assessment of calcium dependency, inhibition by mannose/galactose, and requirement for glycosylation in TSHR-ManR interactions.
  • Evaluation of the effect of ManR binding on in vitro immune responses of splenocytes from TSHR-immunized mice.

    • Main Results:

    • CRD4-7-Fc exhibited the highest binding to TSHR, followed by Tg, with minimal binding to TPO.
    • CR-Fc showed binding to Tg but not to TSHR or TPO.
    • TSHR-CRD4-7-Fc interaction was calcium-dependent, inhibited by mannose, and required a glycosylated TSHR A-subunit.
    • Precomplexing TSHR A-subunit with CRD4-7-Fc or adding mannose reduced splenocyte responses.

    Conclusions:

    • The mannose receptor (ManR) likely participates in autoimmune responses against TSHR and Tg, but not TPO.
    • ManR binding to glycosylated TSHR A-subunits provides a mechanism for antigen-presenting cells to capture shed thyroid proteins.
    • This interaction may be significant in the pathogenesis of thyroid autoimmune diseases.