Decrease of Peripheral Large Granular Lymphocytes in Graves' Disease

Iwatani, Yoshinori; Amino, Nobuyuki; Mori, Hidemitsu; Tamaki, Haruo; Aozasa, Mieko; Kabutomori, Osamu; Mori, Masaki; Takahashi, Osamu; Miyai, Kiyoshi

doi:10.1016/b978-0-12-731950-6.50033-4

Cited by 10 publications

(17 citation statements)

References 17 publications

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“…Thus, the increase in CD5^ B ceiis may be important in stimulative immunologic activity against thyroid tissue. The relalive decrease in non-T, non-B eells observed in the stimulative Ihyroloxicosis of Graves' disease is consistent with our previous finding that large granular lymphocytes decrease in thyrotoxic Graves' disease (38]. and may indirectly increase stimulative changes in thyroid tissue by reduction of kilier and NK cell eytotoxieity [39].…”

Section: Discussionsupporting

confidence: 79%

Decreases in αβ T cell receptor negative T cells and CD8 cells, and an increase in CD4 +CD8+ cells in active Hashimoto's disease and subacute thyroiditis

Iwatani

Amino

Hidaka

et al. 1992

Clinical and Experimental Immunology

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SUMMARY We examined peripheral lymphocyte subsets in patients with autoimmune thyroid disease, or subacute thyroiditis, in the active stage when possible. During destructive thyrotoxicosis arising from aggravation of Hashimoto's thyroiditis, both the numbers and proportions of αβ T cell receptor (TCR) negative T (WT31− CD3+) cells and CD8 (CD4− CD8+) cells decreased and those of CD4+ CD8+ cells increased slightly, resulting in proportional increases in CD4 (CD4+ CD8−) cells. non‐T, non‐B (CD5− CD19−) cells, and the CD4/CD8 cell ratio. Changes were similar in active subacute thyroiditis. During stimulative thyrotoxicosis in active Graves' disease, the numbers of such T lymphocyte subsets were not changed, but only the number of CD5+ B (CD5+CD19+) cells increased markedly, resulting in proportional decreases in total T (CD3+) cells, αβ+ TCR T (WT31+ CD3+) cells, CD8 cells, and non‐T, non‐B cells. A serial study of some of the patients showed opposite changes in αβ TCR− T cells, the CD4/CD8 cell ratio, and CD5+ B cells between the active stages of Graves' and Hashimoto's diseases. αβ TCR− T cells were mostly γδ TCR+ T (IIF2+ CD3+) cells in these patients. These data suggest that αβ TCR T (γδTCR+ T), CD8, and CD4+ CD8+ cells are important in thyroid destruction in Hashimoto's disease and subacute thyroiditis, and that CD5+ B cells arc important in thyroid stimulation in Graves' disease.

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Section: Discussionsupporting

confidence: 79%

Decreases in αβ T cell receptor negative T cells and CD8 cells, and an increase in CD4 +CD8+ cells in active Hashimoto's disease and subacute thyroiditis

Iwatani

Amino

Hidaka

et al. 1992

Clinical and Experimental Immunology

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“…K cells, measured as antibody-dependent cell-mediated cytotoxicity, were found to be normal in thyrotoxic Graves' disease by one group (3) but reduced as quantitated by another (4,5,9). Amino (4) and Iwatani (5) and their colleagues identified reduced NK/ K cell numbers in Graves' disease, with an increase in Hashimotos' disease, and a significant negative correlation with T4 concentration when both diagnostic groups were combined; quantitation was by a plaque-forming technique (4) and by enumeration of LGL cells (5). Using the antibody Leu-7, that may be a specific antibody to NK cells (1, 2), Amino et al recently reported in abstract (9) data comparable to those they obtained with the other procedures (4,5).…”

Section: Discussionmentioning

confidence: 99%

“…This is in part because of the recognized ability of NK cells to interact with other immune cells (28) and to secrete lymphokines such as interferon and IL-2, which have immunoregulatory functions. In this regard there have been considerations that alteration in NK cell activity might be a factor in the perpetuation of Graves' disease (4,5,9). This concept rests on the implication that NK cells (9) [or K cells (4) or LGL (5)] might specifically control the B cells responsible for production of the thyroid-stimulating antibody of Graves' disease (28) and a reduction in cytolytic activity might allow perpetuation of B cell activation.…”

Section: Discussionmentioning

confidence: 99%

“…tolytic assay (6,7) or phenotypic marker (8)(9)(10). Perhaps in part due to the variety oftechniques used, there is a lack of uniformity of results and, specifically in hyperthyroidism, the cytolytic activity or concentration of peripheral blood NK/K cells has been reported as higher than normal (3), normal (8), or decreased (4,5,9).…”

Section: Introductionmentioning

confidence: 99%

“…Reports relevant to an understanding of a role for NK cells in the pathogenesis of autoimmune thyroid disease include studies of K cells (3,4), LGL (5), and NK cells directly by cy-1. Abbreviations used in this paper: E/T, effector/target ratio; IL-2, interleukin 2; LGL, large granular lymphocytes; LU, lytic units; NK, natural killer cells; PBL, peripheral blood lymphocytes; PHA, phytohemagglutinin; PTU, propylthiouracil; TSH, thyrotropin-stimulating hormone; T4, thyroxine.…”

Section: Introductionmentioning

confidence: 99%

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Suppression of peripheral blood natural killer cell activity by excess thyroid hormone.

Papić¹,

Stein‐Streilein²,

Zakarija³

et al. 1987

J. Clin. Invest.

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Natural killer (NK) cells were assessed in patients with hyperthyroxinemia due to Graves' disease or treatment with thyroxine (T4). Cytolytic activity was measured with 5ICr-labeled K562 tumor cells and NK enumeration was by flow cytometry using NKH-1 monoclonal antibody to identify the relevant surface marker. Activity was uniformly decreased in association with hyperthyroxinemia, regardless of the underlying pathology; however, there was no reduction in the number of NKH-1' cells.

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Natural killer cell and islet killer cell activities in Type 1 (insulin-dependent) diabetes

et al. 1986

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Peripheral blood mononuclear cells from 20 Type 1 (insulin-dependent) diabetic patients were examined for natural killer cell activity using the K562 cell line as 51Cr labeled targets. Mean natural killer cell cytotoxicity mediated by enriched non-T cells from patients (37 +/- 4.0%) was lower (p less than 0.03) than in controls (56 +/- 3.7%). Specificity was evaluated by examining other patient subgroups. Mean non-T cell mediated natural killer cell activity in Type 2 (non-insulin-dependent) diabetic patients and Type 1 patients with long term disease was 65 +/- 5.4% and 62 +/- 4.8% respectively (p less than 0.003 vs new onset Type 1 patients). Longitudinal studies of new onset Type 1 patients during the remission (honeymoon) phase revealed persistently impaired natural killer cell activity in 3 of 4 patients. In 30 new onset and 11 remission Type 1 diabetic patients, mean non-T cell-mediated cytotoxicity was also measured using dispersed 51Cr labeled islet target cells. Mean islet cytotoxicity mediated by cells from new onset patients was 34 +/- 2.4%, whereas in non-diabetic control subjects mean cytotoxicity was 25 +/- 1.8% (p less than 0.005). During remission, islet cytotoxicity remained at similar or elevated levels in most patients. In patients evaluated simultaneously for K562 and islet cell cytotoxicity, natural killer cell activity was decreased, whereas islet killing was increased. These results suggest a dichotomy in natural killer cell and islet killer cell activities in new onset Type 1 diabetes that could have an important role in the pathogenesis of Type diabetes.

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Decrease of Peripheral Large Granular Lymphocytes in Graves' Disease

Cited by 10 publications

References 17 publications

Decreases in αβ T cell receptor negative T cells and CD8 cells, and an increase in CD4 +CD8+ cells in active Hashimoto's disease and subacute thyroiditis

Decreases in αβ T cell receptor negative T cells and CD8 cells, and an increase in CD4 +CD8+ cells in active Hashimoto's disease and subacute thyroiditis

Suppression of peripheral blood natural killer cell activity by excess thyroid hormone.

Natural killer cell and islet killer cell activities in Type 1 (insulin-dependent) diabetes

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