Stimulating effect of triiodothyronine on cell-mediated immunity

Balázs, Csaba; Leövey, A; Szabó, Mária; Bakó, G

doi:10.1007/bf00561672

Cited by 41 publications

(23 citation statements)

References 9 publications

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“…Others found rapid stimulation of oxygen consumption in human mononuclear blood cells by T 2 (Kvetny 1992). Furthermore, T 3 treatment of healthy volunteers caused significant increase in the phagocytic capacity and the chemiluminescent activity of PMNLs (Balazs et al 1980). Some results in hyperthyroid patients also suggest that thyroid hormone might influence oxygen free-radical formation.…”

Section: Discussionmentioning

confidence: 98%

“…Many years ago, increased metabolic activities in polymorphonuclear leukocytes (PMNLs) of hyperthyroid patients were described (Balazs et al 1980). Alterations in the respiratory burst and arachidonic acid metabolism in PMNLs of patients with thyroid disorders have also been demonstrated (Videla et al 1993, Szabo et al 1996, Magsino et al 2000.…”

Section: Introductionmentioning

confidence: 99%

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Nongenomic effect of thyroid hormone on free-radical production in human polymorphonuclear leukocytes

Mezősi¹,

Szabó²,

Nagy³

et al. 2005

Journal of Endocrinology

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Over the past few years increasing evidence has suggested the nongenomic effects of thyroid hormone, such as the activation of the signal transduction pathways and the activation of nuclear factor-B by the induction of oxidative stress. The present study was undertaken to investigate the effect of thyroid hormone on human polymorphonuclear leukocytes (PMNLs) which are known as important sources of reactive oxygen species in the circulation. The production of superoxide anion (O 2 ) and the activity of myeloperoxidase were determined in the presence and absence of several inhibitors of the signalling pathway. -Thyroxine (T 4 ), L-3,5,3 -tri-iodothyronine (T 3 ) and L-3,5-di-iodothyronine (T 2 ) stimulated O 2 production in PMNLs in a dose-dependent manner within a few minutes of addition to cells. Thyroid hormone-stimulated O 2 production was partially inhibited by pertussis toxin, an inhibitor of GTP-binding G protein, and was completely abolished by the protein kinase C inhibitors calphostin C and Ro-32-0432, and by a calcium chelator (BAPTA; bis-(o-aminophenoxy)ethane-N,N,N ,N -tetraacetic acid). Thyroid hormone stimulated myeloperoxidase activity and induced 125 I incorporation into PMNLs. Furthermore, thyroid hormone pre-incubation enhanced O 2 production for n-formyl-methionyl-leucylphenylalanine (FMLP) stimulation. In conclusion, novel nongenomic actions of thyroid hormone, the induction of superoxide anion production and the stimulation of myeloperoxidase activity in PMNLs were demonstrated. The induction of O 2 production requires calcium and is mediated by a pertussis toxin-sensitive G protein via stimulation of protein kinase C(s). These results suggest the existence of a membrane-bound binding site for thyroid hormone in PMNLs and a physiological role for thyroid hormone in the cellular defence mechanisms by stimulating free-radical production.

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Section: Discussionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

Nongenomic effect of thyroid hormone on free-radical production in human polymorphonuclear leukocytes

Mezősi¹,

Szabó²,

Nagy³

et al. 2005

Journal of Endocrinology

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“…However, a direct effect of T 3 on macrophages and granulocytes has been reported in a number of systems. Indeed, thyroid hormones modulate the metabolism and the functions of purified rat macrophages (48,49) and stimulate phagocytosis by purified human polymorphonuclear granulocytes (50). Moreover, the production of TSH by cultured monocytes following thyrotropin-releasing factor stimulation is inhibited by T 3 (51).…”

Section: Multiple Levels Of T 3 Actions On the Immune System Developmentmentioning

confidence: 99%

Effects of T3Rα1 and T3Rα2 Gene Deletion on T and B Lymphocyte Development

Arpin

Pihlgren

Fraichard

et al. 2000

The Journal of Immunology

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Thyroid hormones bind to several nuclear receptors encoded by T3Rα and T3Rβ genes. There is now accumulating evidence that thyroid hormones act on the immune system. Indeed, mice deficient for thyroid hormones show a reduction in lymphocyte production. However, the mechanisms involved and, in particular, the role of the different thyroid hormone receptors in lymphocyte development have not been investigated. To address that question, we have studied lymphocyte development in mice deficient for the T3Rα1 and T3Rα2 gene products. A strong decrease in spleen cell numbers was found compared with wild-type littermates, B lymphocytes being more severely affected than T lymphocytes. A significant decrease in splenic macrophage and granulocyte numbers was also found. In bone marrow, a reduction in CD45+/IgM− pro/pre-B cell numbers was found in these mice compared with wild-type littermates. This decrease seems to result from a proliferation defect, as CD45+/IgM− cells incorporate less 5-bromo-2′-deoxyuridine in vivo. To define the origin of the bone marrow development defect, chimeric animals between T3Rα−/− and Rag1−/− mice were generated. Results indicate that for B cells the control of the population size by T3Rα1 and T3Rα2 is intrinsic. Altogether, these results show that T3Rα1 or T3Rα2 gene products are implicated in the control of the B cell pool size.

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“…Exercise (swimming) increases phagocytosis and thyroid hormones are responsible for it [56]. Triiodothyronine (T3) stimulated granulocytes' phagocytic activity [57,58]. Melatonin increased engulfment of latex beads [59].…”

Section: Amino Acid Hormonesmentioning

confidence: 99%

Is there a hormonal regulation of phagocytosis at unicellular and multicellular levels? A critical review

Csaba

2017

AMicr

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Phagocytosis is an ancient cell function, which is similar at unicellular and multicellular levels. Unicells synthesize, store, and secrete multicellular (mammalian) hormones, which influence their phagocytosis. Amino acid hormones, such as histamine, serotonin, epinephrine, and melatonin stimulate phagocytosis, whereas peptide hormones, such as adrenocorticotropic hormone (ACTH), insulin, opioids, arginine vasopressin, and atrial natriuretic peptide decreased it, independently on their chemical structure or function in multicellulars. Macrophage phagocytosis of multicellulars is also stimulated by amino acid hormones, such as histamine, epinephrine, melatonin, and thyroid hormones, however, the effect of peptide hormones is not uniform: prolactin, insulin, glucagon, somatostatin, and leptin have positive effects, whereas ACTH, human chorionic gonadotropin, opioids, and ghrelin have negative ones. Steroid hormones, such as estrogen, hydrocortisone, and dexamethasone are stimulating macrophage phagocytosis, whereas progesterone, aldosterone, and testosterone are depressing it. Considering the data and observations there is not a specific phagocytosis hormone, or a hormonal regulation of phagocytosis neither unicellular, nor multicellular level, however, hormones having specific functions in multicellulars also influence phagocytosis at both levels universally (in unicellulars) or individually (in macrophages). Nevertheless, the hormonal influence cannot be neglected, as phagocytosis (as a function) is rather sensitive to minute dose of hormones and endocrine disruptors. The hormonal influence of phagocytosis by macrophages can be deduced to the events at unicellular level.

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Stimulating effect of triiodothyronine on cell-mediated immunity

Cited by 41 publications

References 9 publications

Nongenomic effect of thyroid hormone on free-radical production in human polymorphonuclear leukocytes

Nongenomic effect of thyroid hormone on free-radical production in human polymorphonuclear leukocytes

Effects of T3Rα1 and T3Rα2 Gene Deletion on T and B Lymphocyte Development

Is there a hormonal regulation of phagocytosis at unicellular and multicellular levels? A critical review

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