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

Papić, Miloš; Stein‐Streilein, Joan; Zakarija, M.; McKenzie, J M; Guffee, J; Fletcher, Mary A

doi:10.1172/jci112826

Cited by 61 publications

(28 citation statements)

References 24 publications

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“…This observation is in agreement with the published study of Corrales et al and others (15,26,27), who underlined that the decrease in cytolytic activity in patients with hyperthyroidism could be a consequence of a metabolic effect of thyroid hormones on the number and function of CD16/56 cell populations. Abnormal distribution of NK cell subsets was also observed at the diagnosis of different autoimmune diseases such as multiple sclerosis and lupus erythematosus and was associated with the onset of clinical symptoms of the disease (12,13).…”

Section: Discussionsupporting

confidence: 93%

Analysis of Circulating T γ/δ Lymphocytes and CD16/56 Cell Populations in Children and Adolescents with Graves' Disease

2003

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Section: Discussionsupporting

confidence: 93%

Analysis of Circulating T γ/δ Lymphocytes and CD16/56 Cell Populations in Children and Adolescents with Graves' Disease

2003

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“…Moreover, the measurement of NK activity in PBL from GD patients by cytolytic assay or phenotypic analysis has produced widely different results, with reports of the activity being enhanced (21), normal (22,23) or decreased (24)(25)(26)(27). The reduced effector activity in PBL from hyperthyroid patients would seem to be due to a functional defect rather than to a decreased NK cell count, and the incubation of PBL of GD patients with recombinant human interleukin-2 (rhIL-2) promptly reverses the NK cell defect (27).…”

Section: Introductionmentioning

confidence: 99%

Defect of a subpopulation of natural killer immune cells in Graves’ disease and Hashimoto’s thyroiditis: normalizing effect of dehydroepiandrosterone sulfate

Solerte

Precerutti²,

Gazzaruso³

et al. 2005

eur j endocrinol

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Background: The study of the natural killer (NK) immune compartment could provide important findings to help in the understanding of some of the pathogenetic mechanisms related to autoimmune thyroid diseases (Graves' disease (GD) and Hashimoto's thyroiditis (HT)). Within this context, it was suggested that alterations in NK cell cytotoxicity (NKCC) and NK production of cytokines might occur in subjects with GD and HT, whereas the normalization of NK functions could potentially contribute to the prevention of the onset or the progression of both diseases. Objective: Due to the hypothesis of alterations in NK in autoimmune thyroid diseases, we were interested to evaluate NKCC in GD and HT patients and to modulate NK function and secretory activity with cytokines and dehydroepiandrosterone sulfate (DHEAS) in an attempt to normalize NK cell defect. Design: We studied 13 patients with recent onset Graves' disease, 11 patients with Hashimoto's thyroiditis at first diagnosis and 15 age-matched healthy subjects. Methods: NK cells were concentrated at a density of 7.75 £ 10 6 cells/ml by negative immunomagnetic cell separation and validated by FACScan as CD16 þ /CD56 þ cells. NK cells were incubated with interleukin-2 (IL-2) and interferon-b (IFN-b) and co-incubated with DHEAS at different molar concentrations for measuring NKCC and the secretory pattern of tumor necrosis factor-a (TNF-a) from NK cells. Results: Lower spontaneous, IL-2-and IFN-b-modulated NKCC was demonstrated in GD and HT patients compared with healthy subjects (P , 0.001). A decrease in spontaneous and IL-2-modulated TNF-a release from NK cells was also found in both groups of patients (P , 0.001). The co-incubation of NK cells with IL-2/IFN-b þ DHEAS at different molar concentrations (from 10 28 to 10 25 M/ml/NK cells) promptly normalized NKCC and TNF-a secretion in GD and HT patients. Conclusions: A functional defect of a subpopulation of NK immune cells, involving both NKCC and the secretory activity, was demonstrated in newly-diagnosed GD and HT patients. This defect can be reversed by a dose-dependent treatment with DHEAS. The impairment of NK cell activity in autoimmune thyroid diseases could potentially determine a critical expansion of T/B-cell immune compartments leading to the generation of autoantibodies and to the pathogenesis of thyroid autoimmunity.

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“…Several abnormalities of the immune system have been described in GD patients, either within the thyroid gland (2,3) or in the peripheral blood (4)(5)(6)(7)(8)(9)(10)(11)(12). CD16/56þ cells have rarely been analyzed in GD patients (10)(11)(12)(13).…”

Section: Introductionmentioning

confidence: 99%

Serial analysis of the effects of methimazole or radical therapy on circulating CD16/56 subpopulations in Graves' disease

Rojano

Sasian²,

Gavilán³

et al. 1998

European Journal of Endocrinology

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The distribution of peripheral blood CD16/56 cytotoxic T and natural killer (NK) cells in Graves' disease patients is analyzed in order to correlate them with disease activity and with prognosis. Eighteen patients with Graves' disease, twenty-four patients with Hashimoto's thyroiditis and thirtytwo sex-and age-matched healthy control subjects were studied. Peripheral blood CD16/56 (cytotoxic T and NK) cells were analyzed by cytofluorometry. A decreased proportion of CD16/56þ and CD16/ 56þCD3þ cells were detected in Graves' disease patients when compared with thyroiditis patients and healthy control groups. No correlation was detected with serum free thyroxine. On diagnosis, patients who would require a radical treatment for thyrotoxicosis control showed a significant decrease of cytotoxic CD56þ T (CD3þ) and NK (CD3¹) cells compared with those who would maintain the euthyroid state after methimazole. These results suggest that the cytotoxic compartment, both T and NK cells, of the immune system is altered in patients with Graves' disease, independently of the functional thyroid status. Changes in peripheral blood lymphocytes in Graves' disease patients could be useful as predictive markers of an unfavorable outcome.

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

Cited by 61 publications

References 24 publications

Analysis of Circulating T γ/δ Lymphocytes and CD16/56 Cell Populations in Children and Adolescents with Graves' Disease

Analysis of Circulating T γ/δ Lymphocytes and CD16/56 Cell Populations in Children and Adolescents with Graves' Disease

Defect of a subpopulation of natural killer immune cells in Graves’ disease and Hashimoto’s thyroiditis: normalizing effect of dehydroepiandrosterone sulfate

Serial analysis of the effects of methimazole or radical therapy on circulating CD16/56 subpopulations in Graves' disease

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