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Sandra McLachlan, PhD

Researcher
Co-Director
Thyroid Autoimmunity Laboratory
Cedars-Sinai Medical Center
8700 Beverly Blvd
Los Angeles, California, United States

Sandra McLachlan is a Co-Director of the thyroid autoimmunity laboratory at Cedars-Sinai Medical Center and Professor of medicine at Cedars-Sinai Medical Center. She has been investigating the molecular and cellular basis of thyroid autoimmunity for 35 years. She is internationally recognized as a leader in this field and has published over 220 peer-reviewed papers. Her research focuses on molecular and cellular investigation of immune responses to thyroid peroxidase and thyroglobulin (Hashimoto thyroiditis), and the thyroid stimulating hormone receptor (TSHR; Graves disease). She also studies cloning human auto-antibodies to thyroid peroxidase and thyroglobulin (for antibody epitopic analysis), and the murine model of Graves disease (self-tolerance and genetic susceptiblity).

Dr. McLachlan was the first to demonstrate the in vitro production of autoantoantibodies to thyroglobulin (Tg), thyroid peroxidase (TPO) and the TSHR by patients’ lymphocytes. She also established the thyroid gland as the major site of thyroid autoantibody production, providing the basis for using thyroid tissue from patients with autoimmune thyroid disease in her subsequent cloning of human autoantibodies to TPO and Tg.

Dr. McLachlan has made an indelible mark on the field of thyroidology through her extensive contributions to our understanding of the molecular and cellular basis of thyroid autoimmunity.

Representative Publications:

Antibodies to Thyroid Peroxidase Arise Spontaneously With Age in NOD.H-2h4 Mice and Appear After Thyroglobulin Antibodies.

Breaking Tolerance in Transgenic Mice Expressing the Human TSH Receptor A-Subunit: Thyroiditis, Epitope Spreading and Adjuvant as a ‘Double Edged Sword’.

Shared and Unique Susceptibility Genes in a Mouse Model of Graves’ Disease Determined in BXH and CXB Recombinant Inbred Mice.

The Link Between Graves’ Disease and Hashimoto’s Thyroiditis: A Role For Regulatory T Cells.

Thyrotropin-Blocking Autoantibodies and Thyroid-Stimulating Autoantibodies: Potential Mechanisms Involved in the Pendulum Swinging From Hypothyroidism to Hyperthyroidism or Vice Versa.

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