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Generation of Monoclonal Antibodies Against Natural Products

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Published on: April 6, 2019

A monoclonal thyroid-stimulating antibody.

Takao Ando¹, Rauf Latif, Alla Pritsker

¹Division of Endocrinology, Diabetes, and Bone Diseases, Department of Medicine, Mount Sinai School of Medicine, New York, New York, USA. takao.ando@mssm.edu

The Journal of Clinical Investigation

|December 5, 2002

Summary

A new monoclonal antibody, MS-1, stimulates the thyroid-stimulating hormone receptor (TSHR) without causing receptor cleavage. This finding offers a novel explanation for prolonged thyroid stimulation in Graves disease.

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Area of Science:

Endocrinology
Immunology
Molecular Biology

Background:

The thyrotropin receptor (TSHR) is the primary target in Graves disease.
Stimulating TSHR antibodies, or long-acting thyroid stimulators, cause thyroid overstimulation.

Purpose of the Study:

To clone and characterize a novel monoclonal antibody (MS-1) with TSHR-stimulating activity.
To elucidate the mechanism behind prolonged thyroid stimulation in Graves disease.

Main Methods:

Cloning and characterization of monoclonal antibody MS-1.
Assays measuring TSHR stimulation and antibody binding.
Analysis of TSHR cleavage and receptor degradation.

Main Results:

MS-1 demonstrated thyroid-stimulating activity at low IgG concentrations (20 ng/ml).
MS-1 competed with TSH for binding and stimulation, recognizing a conformational epitope on the TSHR alpha subunit.
Unlike TSH, MS-1 did not enhance TSHR posttranslational cleavage, potentially extending receptor half-life.

Conclusions:

MS-1 provides a new explanation for prolonged thyroid stimulation in Graves disease, linked to impaired TSHR cleavage.
The lack of receptor cleavage by MS-1 may contribute to an extended functional receptor half-life.