title: Analysis of expression and function of the inhibitory receptor ILT2 in lymphocytes from patients with autoimmune thyroid disease.
abstract: OBJECTIVE
  Autoimmune thyroid disease (AITD) is characterized by different defects in immunoregulatory mechanisms. The immunoglobulin-like transcript receptor 2 (ILT2) or leukocyte Ig-like receptor 1 (LIRB1/CD85j) exerts an important immunoregulatory role. We hypothesized that the lymphocytes from AITD patients have a diminished expression and function of ILT2. The aim of this study was to investigate the expression and function of ILT2 in lymphocytes from patients with AITD.
  
  
  METHODS
  In this study, 18 patients with Hashimoto's thyroiditis (HT), 20 with Graves' disease, and 26 healthy controls were studied. ILT2 expression was analyzed by flow cytometry and immunohistochemistry in peripheral blood mononuclear cells (PBMC) and thyroid tissue. The regulatory function of ILT2 was assessed by an assay of inhibition of lymphocyte proliferation and by an analysis of cell cycle progression. The effect of ILT2 on cytokine synthesis was also evaluated.
  
  
  RESULTS
  We found a significant increased expression of ILT2 by lymphocytes in AITD patients. ILT2 was also detected in the leukocyte infiltrate of thyroid tissue from HT patients. On the contrary, a significant diminished inhibitory activity of ILT2 on cell proliferation was observed in AITD patients. In addition, PBMC from AITD patients showed a diminished synthesis of interleukin 10 on ILT2 engagement.
  
  
  CONCLUSIONS
  The abnormal expression and function of ILT2 detected in AITD suggests that this receptor may participate in the pathogenesis of this condition.
authors.affiliation: Department of Immunology, School of Medicine, Universidad Autónoma de San Luis Potosí, Avenue V. Carranza 2405, 78210 San Luis Potosí, S.L.P., Mexico.
authors.forename: Lesly
authors.initials: L
authors.lastname: Doníz-Padilla
authors.forename: Amalia E
authors.initials: AE
authors.lastname: Paniagua
authors.forename: Pilar
authors.initials: P
authors.lastname: Sandoval-Correa
authors.forename: Adriana
authors.initials: A
authors.lastname: Monsiváis-Urenda
authors.forename: Susanna
authors.initials: S
authors.lastname: Leskela
authors.forename: Mónica
authors.initials: M
authors.lastname: Marazuela
authors.forename: Roberto
authors.initials: R
authors.lastname: González-Amaro
mesh_terms: D015703:Antigens, CD / Q000096:biosynthesis* / Q000502:physiology*; D049109:Cell Proliferation / Q000187:drug effects; D006111:Graves Disease / Q000276:immunology*; D050031:Hashimoto Disease / Q000276:immunology*; D006801:Humans; D016753:Interleukin-10 / Q000096:biosynthesis; D000075362:Leukocyte Immunoglobulin-like Receptor B1; D007963:Leukocytes, Mononuclear / Q000187:drug effects / Q000473:pathology; D008214:Lymphocytes / Q000276:immunology*; D011971:Receptors, Immunologic / Q000096:biosynthesis* / Q000502:physiology*; D013961:Thyroid Gland / Q000378:metabolism
chemical_list: D015703:Antigens, CD; C105299:LILRB1 protein, human; D000075362:Leukocyte Immunoglobulin-like Receptor B1; D011971:Receptors, Immunologic; D016753:Interleukin-10