Activated interstitial and intraepithelial thyroid lymphocytes in autoimmune thyroid disease

1988 ◽  
Vol 119 (2) ◽  
pp. 161-166 ◽  
Author(s):  
Shara B. Cohen ◽  
Anthony P. Weetman
Keyword(s):  
T Cells ◽  
Autoimmune Thyroiditis ◽  
Transferrin Receptor ◽  
Autoimmune Thyroid Disease ◽  
Receptor Expression ◽  
Graves Disease ◽  
Follicular Cells ◽  
Autoimmune Thyroid ◽  
Thyroid Follicular Cells ◽  
Transferrin Receptor Expression

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.

Diltiazem inhibits transferrin receptor expression and causes G1 arrest in normal and neoplastic T cells

1986 ◽  
Vol 6 (12) ◽  
pp. 4244-4250
Author(s):  
L M Neckers ◽  
S Bauer ◽  
R C McGlennen ◽  
J B Trepel ◽  
K Rao ◽  
...  
Keyword(s):  
T Cells ◽  
Transferrin Receptor ◽  
Interleukin 2 ◽  
Receptor Expression ◽  
Calcium Flux ◽  
G1 Arrest ◽  
Receptor Mrna ◽  
Interleukin 2 Receptor ◽  
Transferrin Receptor Expression ◽  
Malignant T Cells

Transferrin receptor expression is essential for the proliferation of both normal and malignant T cells. While transferrin receptor expression in normal T cells is tightly coupled to interleukin-2 receptor expression, transferrin receptor expression in malignant cells is usually constitutive and is released from this constraint. Temporally, the appearance of these membrane receptors is preceded by changes in the expression of the proto-oncogenes c-myc and c-myb. In addition, although an increase in the level of intracellular free calcium occurs early in the sequence of T-cell activation, the activation events dependent on this calcium flux have not been resolved. In the present study we report that diltiazem, an ion channel-blocking agent that inhibits calcium influx, arrested the growth in vitro of both normal and malignant human T cells in the G1 phase of the cell cycle. However, diltiazem did not inhibit the expression of c-myc or interleukin-2 receptor mRNA and protein in normal mitogen-activated T cells or the constitutive expression of c-myc and c-myb mRNA in malignant T cells (T acute lymphoblastic leukemia cells). In contrast, diltiazem prevented the induction of transferrin receptor (mRNA and protein) in normal T cells and caused a progressive loss of transferrin receptor (mRNA and protein) in malignant T cells. These data demonstrate that diltiazem can dissociate several growth-related processes normally occurring in G1 and thereby disrupt the biochemical cascade leading to cell proliferation.

scholarly journals Diltiazem inhibits transferrin receptor expression and causes G1 arrest in normal and neoplastic T cells.

1986 ◽  
Vol 6 (12) ◽  
pp. 4244-4250 ◽  
Author(s):  
L M Neckers ◽  
S Bauer ◽  
R C McGlennen ◽  
J B Trepel ◽  
K Rao ◽  
...  
Keyword(s):  
T Cells ◽  
Transferrin Receptor ◽  
Interleukin 2 ◽  
Receptor Expression ◽  
Calcium Flux ◽  
G1 Arrest ◽  
Receptor Mrna ◽  
Interleukin 2 Receptor ◽  
Transferrin Receptor Expression ◽  
Malignant T Cells

Transferrin receptor expression is essential for the proliferation of both normal and malignant T cells. While transferrin receptor expression in normal T cells is tightly coupled to interleukin-2 receptor expression, transferrin receptor expression in malignant cells is usually constitutive and is released from this constraint. Temporally, the appearance of these membrane receptors is preceded by changes in the expression of the proto-oncogenes c-myc and c-myb. In addition, although an increase in the level of intracellular free calcium occurs early in the sequence of T-cell activation, the activation events dependent on this calcium flux have not been resolved. In the present study we report that diltiazem, an ion channel-blocking agent that inhibits calcium influx, arrested the growth in vitro of both normal and malignant human T cells in the G1 phase of the cell cycle. However, diltiazem did not inhibit the expression of c-myc or interleukin-2 receptor mRNA and protein in normal mitogen-activated T cells or the constitutive expression of c-myc and c-myb mRNA in malignant T cells (T acute lymphoblastic leukemia cells). In contrast, diltiazem prevented the induction of transferrin receptor (mRNA and protein) in normal T cells and caused a progressive loss of transferrin receptor (mRNA and protein) in malignant T cells. These data demonstrate that diltiazem can dissociate several growth-related processes normally occurring in G1 and thereby disrupt the biochemical cascade leading to cell proliferation.

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
Keyword(s):  
Multinodular Goiter ◽  
Class Ii ◽  
Hla Class Ii ◽  
Follicle Cells ◽  
Graves Disease ◽  
Follicular Cells ◽  
Autoimmune Thyroid Diseases ◽  
Autoimmune Thyroid ◽  
Hla Dr ◽  
Thyroid Follicular Cells

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.

scholarly journals PD-1/PD-L1 Expressions on Treg Cells in Patients with Autoimmune Thyroid Disease

2021 ◽  
Author(s):  
Lin Cui ◽  
Xiaotong Gu ◽  
Haixia Liu ◽  
Hong Zheng
Keyword(s):  
T Cells ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Peripheral Blood ◽  
Thyroid Disease ◽  
Autoimmune Thyroid Disease ◽  
Treg Cells ◽  
Graves Disease ◽  
Newly Diagnosed ◽  
Autoimmune Thyroid

Abstract Background: Autoimmune thyroid disease(AITD) is a frequent autoimmune disease characterized by lymphocytic infiltration and thyroid autoantibody production caused by autoimmune dysfunction. Recent studies have shown that Treg cells can participate in the pathogenesis of AITD by inhibiting peripheral reactive T cells and thereby inhibiting the autoimmune responses. Programmed cell death-1 (PD-1)/programmed cell death ligand (PD-L1) pathway is a negative costimulatory pathway discovered in recent years, enhancing or blocking this pathway is associated with the immune process of AITD. PD-1/PD-L1 was simultaneously expressed on Treg cells. In this paper, the role of regulatory T cells and PD-1/PD-L1 signaling pathway in AITD was discussed.Methods: We detected the percentage of CD4+CD25+CD127lowT cells, the ratio of PD-1+Treg cells and PD-L1+Treg cells in peripheral blood of twenty patients newly diagnosed with graves disease (GD) and twenty-one patients newly diagnosed with Hashimotos’thyroiditis (HT) patients by flow cytometry, and samples from twenty healthy individuals served as control.Results: The results demonstrated that the proportion of CD4+CD25+CD127lowT cells in peripheral blood of HT patients was lower than that of healthy controls(HCs), the ratio of PD-1+Treg cells of HT patients was higher than that of the HCs and GD patients, the ratio of PD-1+Treg cells of GD patients was higher than that of the HCs, the ratio of PD-L1+Treg cells in Treg cells of HT patients was higher than that of the HCs and GD patients and the ratio of PD-L1+Treg cells of GD patients was higher than that of the HCs. All the above were statistically significant.Conclusions: The treg cells play an obvious role in hashimoto's thyroiditis, but not obvious in Graves' disease.

scholarly journals Overexpression of Metallothionein I/II: A New Feature of Thyroid Follicular Cells in Graves' Disease

2012 ◽  
Vol 97 (2) ◽  
pp. 446-454 ◽  
Author(s):  
M. Ruiz-Riol ◽  
M. J. Martínez-Arconada ◽  
N. Alonso ◽  
B. Soldevila ◽  
D. Marchena ◽  
...  
Keyword(s):  
Graves Disease ◽  
Follicular Cells ◽  
Thyroid Follicular Cells ◽  
New Feature

Decreased transferrin receptor expression by neuromelanin cells in restless legs syndrome

Neurology ◽  
2004 ◽  
Vol 62 (9) ◽  
pp. 1563-1567 ◽  
Author(s):  
J. R. Connor ◽  
X. S. Wang ◽  
S. M. Patton ◽  
S. L. Menzies ◽  
J. C. Troncoso ◽  
...  
Keyword(s):  
Restless Legs Syndrome ◽  
Transferrin Receptor ◽  
Receptor Expression ◽  
Restless Legs ◽  
Transferrin Receptor Expression
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