title: Intrathyroidal accumulation of T cell phenotypes in autoimmune thyroid disease.
abstract: In this study we have correlated peripheral T cell subset phenotypes with intrathyroidal lymphocyte accumulation in patients with autoimmune thyroid disease (Graves' and Hashimoto's disease). Our study utilized euthyroid family members for one of our control groups (n = 48) thus significantly limiting familial, but not disease-specific, influences on these T cell phenotypes. Our principal new observations were found only in patients with Graves' disease. As previously reported, there was a decrease in CD8+ (suppressor/cytotoxic) T cells in the peripheral blood of patients with untreated hyperthyroid Graves' disease (n = 27) (mean +/- SEM, 19 +/- 1.1% in patients compared with 25 +/- 1.2% in controls, p = 0.03), a finding not observed in treated, euthyroid Graves' disease patients or their relatives. However, the relative number of CD8+ T cells, assessed by CD4:CD8 ratios, was increased in the intrathyroidal T cell populations (n = 10), when compared to normal and patient peripheral blood. There were no consistent changes in total CD4+ (helper) T cells in the peripheral blood of patients with treated and untreated Graves' disease but a reduction in CD4+2H4+ (suppressor-inducer) T cells was seen in patients undergoing surgery for Graves' disease (13 +/- 6.9% compared with 39 +/- 3.4%). Again, however, this T cell subset was increased within the target organ of the same patients (41 +/- 5.9%). These data point to either a selective accumulation, or a specific "homing", of certain T cell subsets within the thyroid gland of patients with Graves' disease where T cell differentiation may be strongly influenced by antithyroid drug treatment and the local immune environment.
authors.affiliation: Department of Medicine, Mount Sinai School of Medicine, New York, New York.
authors.forename: A
authors.initials: A
authors.lastname: Martin
authors.forename: N K
authors.initials: NK
authors.lastname: Goldsmith
authors.forename: E W
authors.initials: EW
authors.lastname: Friedman
authors.forename: A E
authors.initials: AE
authors.lastname: Schwartz
authors.forename: T F
authors.initials: TF
authors.lastname: Davies
authors.forename: S H
authors.initials: SH
authors.lastname: Roman
mesh_terms: D013956:Antithyroid Agents / Q000494:pharmacology / Q000627:therapeutic use; D001323:Autoantibodies / Q000032:analysis; D001327:Autoimmune Diseases / Q000235:genetics / Q000276:immunology / Q000473:pathology* / Q000628:therapy; D002454:Cell Differentiation; D002634:Chemotaxis, Leukocyte; D006111:Graves Disease / Q000235:genetics / Q000276:immunology / Q000473:pathology* / Q000628:therapy; D006684:HLA-DR Antigens / Q000276:immunology; D006801:Humans; D018828:Immunoglobulins, Thyroid-Stimulating; D007958:Leukocyte Count; D016176:T-Lymphocyte Subsets / Q000276:immunology / Q000473:pathology*; D013961:Thyroid Gland / Q000276:immunology / Q000473:pathology*; D013965:Thyroidectomy; D013967:Thyroiditis, Autoimmune / Q000235:genetics / Q000276:immunology / Q000473:pathology* / Q000628:therapy
chemical_list: D013956:Antithyroid Agents; D001323:Autoantibodies; D006684:HLA-DR Antigens; D018828:Immunoglobulins, Thyroid-Stimulating; C056626:thyroid microsomal antibodies