Review and hypothesis: does Graves' disease develop in non-human great apes?

Area of Science:

• Endocrinology
• Immunology
• Evolutionary Biology

Background:

• Graves' disease, an autoimmune disorder targeting the thyrotropin receptor (TSHR), is not observed in animals.
• TSHR glycosylation varies across species, with humans and great apes having more N-glycans than other placental mammals.
• This difference in glycosylation may influence the immunogenicity of the TSHR A-subunit, the primary autoantigen in Graves' disease.

Purpose of the Study:

• To investigate the hypothesis that reduced TSHR A-subunit glycosylation in most placental mammals accounts for the absence of Graves' disease.
• To explore whether great apes, with human-like TSHR glycosylation, might develop Graves' disease.
• To analyze existing literature and survey veterinarians regarding thyroid dysfunction in great apes.

Main Methods:

• Literature review on TSHR autoantibodies and glycosylation.
• Survey of veterinarians at North American primate centers and zoos.
• Analysis of reported cases of thyroid dysfunction in great apes.

Main Results:

• Literature search identified limited cases of thyroid dysfunction in great apes, with only one instance of hyperthyroidism (a deceased gorilla).
• A survey of 979 chimpanzees and approximately 1100 other great apes in U.S. facilities revealed no diagnoses of noncongenital thyroid dysfunction or hyperthyroidism.
• Only three hypothyroid cases were reported among the surveyed great apes.

Conclusions:

• Graves' disease appears to be very rare or absent in great apes, based on current literature and survey data.
• The hypothesis that human-like TSHR glycosylation in great apes leads to Graves' disease is not supported by the available evidence.
• Further research with larger sample sizes and comprehensive thyroid function/autoantibody testing is needed to confirm if Graves' disease is exclusively a human condition.