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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The formation of macrophage-lymphocyte rosettes was studied in lymphocyte cultures from patients with Graves' disease; Hashimoto's thyroiditis, other thyroid diseases and control subjects; the cultures were incubated with normal human thyroid and other non-specific antigens. At the end of incubation, the cell pellets were smeared on slides, stained with Wright's stain and the number of rosettes determined under the microscope. The membrane immunofluorescence technique was employed to identify whether the surrounding lymphocytes were T- or B-lymphocytes. In Graves' disease and Hashimoto's thyroiditis, the mean percentages of rosette formation with crude thyroid antigen were 0.98 +/- 0.22% (mean +/- SEM), and 1.15 +/- 0.25%, respectively. These values were significantly higher than those of control lymphocytes (0.03 +/- 0.02%). Lymphocytes from other thyroid diseases also gave higher values than controls. Kidney antigen, used as a control antigen, gave negative results in Graves' disease and other thyroid diseases, but in Hashimoto's thyroiditis, the mean percentage was of borderline significance. In the direct immunofluorescent staining study using fluorescein-conjugated goat anti-human Ig determinants, including the Fab fraction of anti-human IgG, it appeared that both B- and T-lymphocytes were involved in the rosettes, although B-lymphocytes were more numerous. These results indicate that in patients with Graves' disease and Hashimoto's thyroiditis, a probable immune reaction with thyroid antigen can be demonstrated by macrophage-lymphocyte rosette formation.
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PMID:Macrophage-lymphocyte interaction in Graves' disease and Hashimoto's thyroiditis. 8 54

We have studied by flow cytometric analysis the antigen specific activation of CD4+ (helper/inducer) T lymphocytes by purified human thyroid peroxidase (TPO). Peripheral blood mononuclear cells were obtained from 26 patients with Graves' disease (GD), 16 with Hashimoto's thyroiditis (HT), 7 with nontoxic nodular goiter (NG), and 14 normal subjects (N). Cells were cultured for 7 days in the presence or absence of TPO at final concentrations of 3, 30, and 300 ng/mL. When harvested, cells were reacted with an FITC-conjugated anti-CD4 and a PE-conjugated anti-HLA-DR murine monoclonal antibodies. The percentage of HLA-DR+ CD4+ cells (activated CD4+ cells) was determined by a flow cytometer. In the absence of TPO, CD4+ cells had been activated without any specific stimulant. This is known as the autologous mixed lymphocyte reaction (AMLR). In the AMLR, CD4+ cells from GD and HT were less activated compared to those from NG and N. Results of TPO-specific activation were expressed as an incremental increase of activated CD4+ cells (II) (percentage of activated CD4+ cells cultured with TPO minus percentage of activated CD4+ cells cultured without TPO). II of N, GD, HT, and NG were 0.37 +/- 0.21, 2.20 +/- 0.45,** 2.0 +/- 0.66,* and 0.35 +/- 0.27 (mean +/- SEM), respectively (**p less than 0.01; *p less than 0.05 vs N). When patients were further subdivided, the highest mean II was found in patients with hyperthyroid GD (p less than 0.01), followed by euthyroid HT (p less than 0.05) and euthyroid GD (p less than 0.05), however there was no significant difference between hypothyroid HT and N. In conclusion (1) AMLR reactivity of CD4+ cells from GD and HT was impaired, (2) however, CD4+ cells from both GD and HT were significantly more induced by TPO compared to N, and (3) this induction depends, in part, on the in vivo thyroid status.
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PMID:Studies of CD4+ (helper/inducer) T lymphocytes in autoimmune thyroid disease: demonstration of specific induction in response to thyroid peroxidase (TPO) in vitro and its relationship with thyroid status in vivo. 168

In this study we have correlated peripheral T cell subset phenotypes with intrathyroidal lymphocyte accumulation in patients with autoimmune thyroid disease (Graves' and Hashimoto's disease). Our study utilized euthyroid family members for one of our control groups (n = 48) thus significantly limiting familial, but not disease-specific, influences on these T cell phenotypes. Our principal new observations were found only in patients with Graves' disease. As previously reported, there was a decrease in CD8+ (suppressor/cytotoxic) T cells in the peripheral blood of patients with untreated hyperthyroid Graves' disease (n = 27) (mean +/- SEM, 19 +/- 1.1% in patients compared with 25 +/- 1.2% in controls, p = 0.03), a finding not observed in treated, euthyroid Graves' disease patients or their relatives. However, the relative number of CD8+ T cells, assessed by CD4:CD8 ratios, was increased in the intrathyroidal T cell populations (n = 10), when compared to normal and patient peripheral blood. There were no consistent changes in total CD4+ (helper) T cells in the peripheral blood of patients with treated and untreated Graves' disease but a reduction in CD4+2H4+ (suppressor-inducer) T cells was seen in patients undergoing surgery for Graves' disease (13 +/- 6.9% compared with 39 +/- 3.4%). Again, however, this T cell subset was increased within the target organ of the same patients (41 +/- 5.9%). These data point to either a selective accumulation, or a specific "homing", of certain T cell subsets within the thyroid gland of patients with Graves' disease where T cell differentiation may be strongly influenced by antithyroid drug treatment and the local immune environment.
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PMID:Intrathyroidal accumulation of T cell phenotypes in autoimmune thyroid disease. 171 76

A sonographic grey scale (gs) analysis of the thyroid gland was retrospectively (1985-1986) performed in 248 patients with normal sized thyroid glands or "diffuse" thyroid diseases. During the examination the physical parameters for gain, far and near gain were constant. The normal value (means +/- 2 s) in 95 patients with normal sized and euthyroid thyroid glands was lower in females (gs: 14 +/- 4) than in males (gs: 16 +/- 6), children had obviously lower patterns (gs: 7.1), adolescents had low normal patterns (gs: 11). The echogenicity increased with increasing thyroid volumes. In patients with autoimmune thyroid diseases an obvious low echogenicity could be demonstrated (Hashimoto's thyroiditis, gs-SEM: 8.3 +/- 1.5; Grave's disease, gs-SEM: 6.7 +/- 1.2) (SEM = standard error of the mean). Euthyroid patients with microsomal antibody titers showed low normal grey scale patterns (gs: 10.9 +/- 3). In patients after subtotal thyroidectomy the grey scale pattern decreased with decreasing volume of the residual thyroid gland. The grey scale pattern increased years after surgery. The subjective grading of the grey scale pattern was different from the quantitatively measured pattern in 18% of the patients with glands of normal size.
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PMID:[The importance of quantitative grey-scale analysis of the sonogram in "diffuse" thyroid diseases]. 253 99

Antibody-dependent cell-mediated cytotoxicity (ADCC) is the process by which antibodies interact with killer cells to effect cell lysis, whereas natural killing (NK) refers to the ability of peripheral blood killer cells to lyse target cells in the absence of specific antibody. The purpose of the present study was to determine if either NK cells or ADCC might play a role in the development of Hashimoto's thyroiditis (HD) by testing the ability of killer cells to cause lysis of K562 erythroleukemia tumor cells and human thyrocytes in the presence and absence of serum from normal and HD patients. Using K562 target cells, NK activity was 70 +/- 4% (mean +/- SEM) for HD effector cells and 66 +/- 5% for normal effector cells at an effector to target ratio of 100:1. Similarly, with thyrocytes as targets, effector cells from HD patients (38 +/- 3%) and normal subjects (34 +/- 5%) caused comparable lysis (at an effector to target ratio of 100:1). Using K562 target cells, ADCC was 35% when effector cells from HD or normal subjects were coincubated with either normal or HD sera. Using thyrocyte target cells, lysis was about 25-30%, but, again, no differences were found between HD and normal effector cells or serum. There was a significant correlation between lysis for K562 and thyrocyte target cells, but there was no significant correlation between the titer of serum antithyroid microsomal antibodies and specific lysis. Intrathyroidal lymphocytes and peripheral lymphocytes from one patient with HD caused comparable lysis of labeled thyrocyte targets, as did normal peripheral lymphocytes. We conclude that ADCC and NK activities in peripheral lymphocytes were normal in HD patients and, therefore, may not have a primary role in mediating thyrocyte destruction in Hashimoto's thyroiditis.
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PMID:Killer cell activity and antibody-dependent cell-mediated cytotoxicity are normal in Hashimoto's disease. 375 62

To investigate the activity of the thyroid gland to convert T4 to T3, we measured the activity of thyroid T4 5'-deiodinase in the following human thyroid glands: 9 normal glands, 5 Hashimoto's thyroiditis, 13 follicular adenomas, 11 methimazole (MMI)-treated Graves' disease (GD), 11 propranolol iodide-treated GD, and 8 propylthiouracil (PTU)-treated GD. The enzyme activity was determined by the ability of 100,000 X g pellet of the thyroid homogenate to convert T4 to T3 in vitro. Normal thyroids showed the enzyme activity of 1.59 +/- 0.18 (mean +/- SEM) pmol T3/mg protein/min. Euthyroid Hashimoto's thyroiditis displayed the enzyme activity of 1.01 +/- 0.15 pmol T3/mg protein/min, which was similar to the normal thyroid enzyme activity. The hypothyroid gland of Hashimoto's thyroiditis showed the enzyme activity of 1.8 pmol T3/mg protein/min. Follicular adenomas showed a wide range of enzyme activity with the mean level of 3.24 +/- 0.82 pmol T3/mg protein/min that did not differ significantly from that of the normal thyroids. Interestingly, one adenoma, despite TSH suppression that ordinarily decreases enzyme activity, showed the greatest activity of 11.0 pmol T3/mg protein/min. Graves' thyroids following treatment with MMI, PTU, and propranolol-iodide showed enzyme activities of 4.61 +/- 0.53, 3.95 +/- 0.43, and 3.51 +/- 0.46 pmol T3/mg protein/min, respectively; all these values were greater than that of the normal thyroids (P less than 0.01), but did not differ significantly when compared with each other. In summary, thyroid glands with Hashimoto's thyroiditis had activities of T4 to T3 conversion similar to the normal thyroid glands.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Thyroid T4 5'-deiodinase activity in normal and abnormal human thyroid glands. 620 Jul 49

Porcine thyroid follicle cells, cultured in suspension, were employed to investigate the effects of immunoglobulin preparations from patients with colloid goitre, Graves' disease or Hashimoto's thyroiditis on thyroid growth in vitro. Epidermal growth factor (EGF, 19 ng/ml) was used as a reference for maximum growth stimulation and produced a 9-fold increase in [3H]thymidine incorporation. Immunoglobulins (1000 micrograms/ml) were found to increase [3H]thymidine incorporation compared to control: from 10 normal individuals 32 +/- 4% (mean +/- SEM, % of EGF response), from 10 patients with colloid goitre 26 +/- 4% (not significantly different from normal), from 10 patients with Graves' disease 19 +/- 3% (P less than 0.05) and from 15 patients with Hashimoto's thyroiditis 11 +/- 2% (P less than 0.001). No patient immunoglobulin preparation showed activity greater than that of normal individuals. The lower growth stimulatory activity in Graves' disease and Hashimoto's thyroiditis remained after heat inactivation of serum and is thought to reflect surface binding of thyroid autoantibodies.
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PMID:Influence of thyroid autoantibodies on thyroid cellular growth in vitro. 660 95

Platelet IgG levels, count, and function and easy bruising or bleeding were studied in 25 patients with Graves' disease and 12 with Hashimoto's thyroiditis (normal value for platelet IgG 10.7 +/- 4.5 ng [SD]/10(6) platelets). Eight of 22 patients with Graves' disease and normal platelet counts had elevated platelet IgG averaging 38 +/- 4.0 ng (SEM) (range, 24 to 60). Four of 10 patients with Hashimoto's thyroiditis and normal platelet counts ahd elevated platelet IgG averaging 45 +/- 7.2 ng (range, 27 to 66). Five patients with thrombocytopenia had platelet counts averaging 53000 +/- 12000/microL (SEM) and elevated platelet IgG averaging 154 +/- 40 ng (range, 27 to 300). Twelve of 15 patients with a history of easy bruising or bleeding had elevated platelet IgG compared to five of 22 without easy bruising (p < 0.001). Four of six with elevated platelet IgG had one or more abnormal in-vitro platelet aggregation measurements (particularly with epinephrine) compared to none of six with normal platelet IgG levels (p = 0.03). We conclude that elevated platelet IgG is associated with easy bruising and thrombocytopenia in about half of patients with Graves' disease or Hashimoto's thyroiditis.
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PMID:Easy bruising, thrombocytopenia, and elevated platelet immunoglobulin G in Graves' disease and Hashimoto's thyroiditis. 689 93

Previous studies indicated that circulating 20 alpha-hydroxyprogesterone (20 alpha-OH-P) in cyclic female rats derived from enzymatic conversion of progesterone in corpus luteum tissue (Hashimoto and Wiest, 1969). A possibility of extraovarian conversion of progesterone to 20 alpha-OH-P also was revealed by our recent finding that placement of Silastic implants of progesterone produced not only high plasma progesterone but also 20 alpha-OH-P in ovariectomized (OVX), previously pseudo-pregnant, rats (Gilman et al., 1981). This study was performed to measure the amounts of serum 20 alpha-OH-P and progesterone in intact or adrenalectomized (ADX), cyclic female rats and in OVX, ADX or OVX-ADX animals with or without progesterone implants. Twenty-four-hour patterns of serum progestins revealed that OVX rats exhibited low progesterone secretion (3-6 ng/ml) and undetectable levels of 20 alpha-OH-P in the absence of ovaries. In intact, cyclic females, circulating concentrations of 20 alpha-OH-P were 4- to 6-fold greater than those or progesterone. ADX resulted in a partial reduction of progesterone but not 20 alpha-OH-P in the circulation. Placement of 4 cm Silastic implants of progesterone produced high serum concentrations of both progesterone (29 +/- 4 ng/ml, mean +/- SEM) and 20 alpha-OH-P (27 +/- 1 ng/ml) in OVX and OVX-ADX rats. These findings demonstrate that placement of progesterone implants into female rats produces high circulating concentrations of both progesterone and 20 alpha-OH-P, and indicate that an extraovarian and extra-adrenal system(s) for progestin conversion is functioning under persistently high circulating progesterone conditions. By this system, large amounts of circulating progesterone are transformed into a less potent progestational compound, 20 alpha-OH-P.
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PMID:Silastic implants of progesterone produce high circulating levels of both progesterone and 20 alpha-hydroxyprogesterone in ovariectomized, adrenalectomized rats. 708 17

We have examined the hTcR V gene family use of T-cells present in the aspiration thyroid biopsy specimens of patients with hyperthyroid Graves' disease (n = 8) and Hashimoto's autoimmune thyroiditis (n = 5). Nine of the 13 specimens had cytologically identified thyroid follicular cells, and 12 of the 13 contained human thyroglobulin-specific mRNA, confirming successful sampling. Of 18 hTcR V alpha and 19 hTCR V beta gene families tested for in the individual aspirates, a mean +/- SEM of 6.8 +/- 0.9 V alpha and 9.6 +/- 1.4 V beta gene families were present in the Graves' aspirates, while 12.2 +/- 1.7 and 16.8 +/- 0.4 V alpha and V beta gene families were present in the aspirates of patients with Hashimoto's thyroiditis. These samples, which offer a window onto the natural history of autoimmune thyroid disease, demonstrate significant hTcR V alpha and beta gene restriction in hyperthyroid Graves' disease, but much less restriction of both V alpha and V beta gene families in Hashimoto's disease. Such data extend our earlier information based only on examination of highly selected surgical specimens of patients with autoimmune thyroid disease to the much more typical patient. We conclude that hTcR V gene restriction of varying degrees is present in the majority of patients with autoimmune thyroid disease, but appears to be more easily detected in Graves', rather that Hashimoto's, disease.
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PMID:T-cell receptor V gene use in autoimmune thyroid disease: direct assessment by thyroid aspiration. 844 22


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