scholarly journals Autoimmune and non-autoimmune thyroid diseases have different patterns of cellular HLA class II expression

1999 ◽  
Vol 117 (4) ◽  
pp. 161-164 ◽  
Author(s):  
Denise Engelbrecht Zantut-Wittmann ◽  
Luís Henrique Barbosa Boechat ◽  
Glauce Aparecida Pinto ◽  
Miriam Aparecida da Silva Trevisan ◽  
José Vassallo

CONTEXT: Surface HLA-DR antigen is usually only expressed by antigen-presenting cells (APC). In autoimmune thyroid disease, follicle cells function as APC, thus expressing HLA-DR. However, non-autoimmune thyroid diseases may also express surface class II antigens. OBJECTIVE: To evaluate the presence and pattern of HLA class II expression in autoimmune and non-autoimmune thyroid disorders. DESIGN: Retrospective: histopathological and immunohistochemical analysis. LOCATION: Referral center, university hospital. SAMPLE: Ten histologically normal thyroids, 11 Graves’ disease, 7 Hashimoto’s thyroiditis, 10 atoxic multinodular goiter and 3 toxic adenomas were analyzed by immunohistochemistry, using a monoclonal antibody anti-HLA-DR. MAIN MEASUREMENTS: The presence of these antigens in thyroid follicular cells and their relation to inflammatory infiltrate was evaluated. The pattern of HLA-DR expression in thyroid follicular cells was analyzed: membrane, cytoplasmic or both. RESULTS: Although HLA-DR antigens were sparsely present in one of the 8 normal thyroids, in 6 of the 9 atoxic multinodular goiter and in 2 of the 3 toxic adenomas a net positivity could be seen in large areas. In all 5 Hashimoto’s thyroiditis and in 7 of the 10 Graves’ disease cases. This expression occurred in follicle cells either in contact with inflammatory cells or not. In non-autoimmune thyroid disease, HLA-DR positivity was essentially cytoplasmic, whereas in Graves’ disease and Hashimoto thyroiditis it was mainly in cell membranes. CONCLUSIONS: It is suggested that the HLA class II expression on the surface of follicle cells could be related to auto-antigen presentation to the immune system by these cells, leading to inflammation.

1988 ◽  
Vol 81 (5) ◽  
pp. 1608-1614 ◽  
Author(s):  
B Grubeck-Loebenstein ◽  
M Londei ◽  
C Greenall ◽  
K Pirich ◽  
H Kassal ◽  
...  

1989 ◽  
Vol 122 (1) ◽  
pp. 185-NP ◽  
Author(s):  
A. P. Weetman ◽  
S. Cohen ◽  
M. W. Makgoba ◽  
L. K. Borysiewicz

ABSTRACT Intercellular adhesion molecule-1 (ICAM-1), hitherto identified on activated B cells, macrophages, dendritic cells, endothelia and certain epithelial cells, serves as a ligand for the lymphocyte function-associated antigen-1 (LFA-1). ICAM-1 binding by LFA-1 enhances the efficiency of lymphocyte-target cell and lymphocyte-accessory cell interactions. We have investigated the in-vitro expression of ICAM-1 by cultured thyroid cells from five patients with Graves' disease using indirect immunofluorescence analysis, and found that 30 ± 11% (mean ± s.d.) of cells were ICAM-1 positive under basal conditions. The proportion of cells which were ICAM-1 positive and the amount of ICAM-1 per cell (assessed by fluorescence intensity) were both increased in all cases by the cytokines γ-interferon, interleukin-1 and tumour necrosis factor. Immunohistochemical analysis of frozen sections from thyroidectomy specimens demonstrated ICAM-1 on thyroid follicular cells in areas of lymphocytic infiltration in patients with Graves' disease (n = 2) or Hashimoto's thyroiditis (n = 2). ICAM-1 was not found in specimens from a patient with a toxic multinodular goitre or a patient with Graves' disease without focal lymphocytic accumulation. These results suggest that the thyroid epithelium may express ICAM-1 as well as major histocompatibility complex class II antigens, such as HLA-DR, in response to locally synthesized cytokines. The enhanced expression of ICAM-1 may render these cells more susceptible as targets for lymphocytemediated cytotoxicity, and together with HLA-DR antigen expression may increase the accessory cell capability of the thyroid follicular cells. Journal of Endocrinology (1989) 122, 185–191


1994 ◽  
Vol 41 (6) ◽  
pp. 599-603 ◽  
Author(s):  
EIYU KATSUREN ◽  
TAKUYA AWATA ◽  
CHIAKI MATSUMOTO ◽  
KUNIHIRO YAMAMOTO

1988 ◽  
Vol 119 (2) ◽  
pp. 161-166 ◽  
Author(s):  
Shara B. Cohen ◽  
Anthony P. Weetman

Abstract. This study has further characterised the thyroid lymphocytic infiltrate in Graves' disease and Hashimoto's thyroiditis. Two population of lymphocytes were identified. The interstitial population occurred as a diffuse and a focal infiltrate; most cells were CD3-positive (T cells) and in 4 of 6 glands CD8 (suppressor-cytotoxic)-positive T cells predominated. The intraepithelial population was CD3-negative, CD8-positive. Both populations also contained a few NK (Leu 11b positive cells) in some glands. Many of the lymphocytes in both populations stained with UCHL1 and RFT2 suggesting that these are primed and activated cells, borne out by staining for transferrin receptor expression. Although thyroid follicular cells were Ia-positive, macrophages and dentritic cells were found in all cases, so that a role for antigen-presentation by all three potential candidates in autoimmune thyroiditis is possible.


Thyroid ◽  
2001 ◽  
Vol 11 (6) ◽  
pp. 575-580 ◽  
Author(s):  
Denise Engelbrecht Zantut-Wittmann ◽  
Marcos Antonio Tambascia ◽  
Miriam Aparecida da Silva Trevisan ◽  
Glauce Aparecida Pinto ◽  
José Vassallo

1990 ◽  
Vol 122 (1) ◽  
pp. 41-48 ◽  
Author(s):  
Yasushi Kawakami ◽  
Nobuaki Kuzuya ◽  
Tsuyoshi Watanabe ◽  
Yasuo Uchiyama ◽  
Kamejirou Yamashita

Abstract. Expression of major histocompatibility complex (MHC) class 2 molecules on the thyroid follicular cells in human autoimmune thyroid diseases has been reported, and is suggested to play a role in the initiation of the autoimmune responses. Interferon γ is known to induce MHC class 2 molecules on cultured thyrocytes. Therefore, we administered recombinant interferon γ to mice to induce MHC class 2 molecule expression in vivo, and investigated the thyroidal changes following MHC class 2 molecule expression. Recombinant interferon γ3 × 105 U, was administered daily, to mice. MHC class 2 molecules, studied by indirect immunohistochemistry, were expressed on the follicular cells on the 2nd to 4th day after the first interferon γ administration and continued thereafter. Serum T4 and T3 concentrations decreased and anti-thyroglobulin antibodies and anti-microsomal antibodies were detected. Lymphocyte infiltrations were observed in the thyroid glands obtained at 28 days, but they were mild. These results suggest that MHC class 2 molecule expression on thyroid follicular cells induces anti-thyroid antibodies and plays an important role in the initiation of autoimmune thyroiditis. However, the progression of the immune response to thyroiditis with lymphocyte infiltration may require some other factor. This new model of autoimmune thyroid disease in mice might be useful to elucidate the pathogenesis of human autoimmune thyroid diseases.


2008 ◽  
Vol 93 (2) ◽  
pp. 591-596 ◽  
Author(s):  
Francesco Latrofa ◽  
Debora Ricci ◽  
Lucia Grasso ◽  
Paolo Vitti ◽  
Lucio Masserini ◽  
...  

Abstract Context: Thyroglobulin (Tg) epitopes of serum Tg autoantibodies (TgAb) have been characterized using inhibition of Tg binding by human monoclonal TgAb in autoimmune thyroid diseases (AITD) [Hashimoto’s thyroiditis (HT) and Graves’ disease (GD)] but not in non-AITD [nontoxic multinodular goiter (NTMG) and papillary thyroid carcinoma (PTC)]. Objective: Our objective was to compare Tg epitopes of serum TgAb from patients with AITD, non-AITD, and PTC associated with histological thyroiditis (PTC-T) using inhibition of Tg binding by four recombinant human TgAb-Fab (epitopic regions A–D). Design: Inhibition of Tg binding of 24 HT, 25 GD, 19 NTMG, 15 PTC, and 25 PTC-T TgAb-positive sera by each TgAb-Fab was evaluated in ELISA. Inhibition by the pool of the four TgAb-Fab was evaluated using labeled Tg. Results: Levels of inhibition were different for TgAb-Fab regions A (P = 0.001), B (0.007), and D (0.011). Inhibition by region A TgAb-Fab was significantly higher in HT, GD, and PTC-T than in NTMG and PTC patients. Inhibition levels by region B TgAb-Fab were significantly higher in HT compared with NTMG and PTC patients and in GD compared with NTMG patients. Inhibition by D region TgAb-Fab was significantly lower in NTMG than in the other groups. Inhibition by the pool ranged from 44% (NTMG) to 72% (GD). Conclusions: The pattern of Tg recognition is similar when HT patients are compared to GD and NTMG to PTC patients and differs when AITD are compared with non-AITD patients. In PTC-T patients, it is similar to that of AITD patients.


2011 ◽  
Vol 4 (1) ◽  
pp. 13 ◽  
Author(s):  
Artur Bossowski ◽  
Jerzy Harasymczuk ◽  
Anna Moniuszko ◽  
Anna Bossowska ◽  
Maciej Hilczer ◽  
...  

1996 ◽  
Vol 135 (1) ◽  
pp. 69-76 ◽  
Author(s):  
Kenji Kashima ◽  
Shigeo Yokoyama ◽  
Tsutomu Daa ◽  
Kenji Takahashi ◽  
Iwao Nakayama ◽  
...  

Kashima K, Yokoyama S, Daa T, Takahashi K, Nakayama I, Noguchi S. c-myc Expression is associated with increased proliferation activity in thyroid follicular cells of Graves' disease as stimulated by autoantibodies. Eur J Endocrinol 1996:135:69–76. ISSN 0804–4643 Expression on thyroid follicular cells of HLA-DR, c-myc protein and proliferating cell nuclear antigen (PCNA) was examined immunohistochemically in 28 cases of Graves' disease (GD) and in 29 cases of Hashimoto's thyroiditis (HT). Immunoreactivity for PCNA in GD was seen not only in follicular cells adjacent to a lymphocytic infiltration, where the follicular cells were positive for HLA-DR, but also in hyperplastic follicular cells without the infiltration. The distribution of expressed c-myc protein was similar to that of PCNA in GD but not in HT. Semiquantitatively graded degrees of lymphocytic infiltration and expression of HLA-DR, c-myc and PCNA in GD showed a high correlation with one another. However, the degrees of c-myc expression in HT showed no significant correlation with any other degrees. Intraperitoneal injection of bovine TSH or of immunoglobulins derived from a patient with GD in rabbits induced hyperplastic change of thyroid follicular cells, as reflected in PCNA and c-myc immunoreactivity, as well as strong peroxidase and acid phosphatase activity. Immunization with synthesized peptide of thyrotropin receptor also exhibited the same results in the rabbit thyroids. Our results indicate that c-myc expression on follicular cells of GD may reflect a stimulation by autoantibodies mediated through the thyrotropin receptor. Kenji Kashima, Department of Pathology, Oita Medical University, 1-1 Oita-gun, Oita 879-55, Japan


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