Cited by 347Thyroid Disorders and TreatmentsImmunotoxicology and immune responsesImmune Response and Inflammation

Thyroid Hormones as Modulators of Immune Activities at the Cellular Level

De Vito, Paolo, Incerpi, Sandra, Pedersen, Jens Z., Luly, Paolo, Davis, Faith B., Davis, Paul J.·2011·Thyroid

Abstract

BACKGROUND: Increasing evidence suggests that thyroid hormones, L-thyroxine (T(4)) and 3,3',5-triiodo-L-thyronine (T(3)), are modulators of the immune response. In monocytes, macrophages, leukocytes, natural killer cells, and lymphocytes, a wide range of immune functions such as chemotaxis, phagocytosis, generation of reactive oxygen species (ROS), and cytokine synthesis and release are altered under hypo- and hyperthyroid conditions. SUMMARY: Hyperthyroidism decreases the proinflammatory activities of monocytes and macrophages, whereas enhancement of phagocytosis and increased levels of ROS may occur during hypothyroidism. The expression of proinflammatory molecules such as macrophage inflammatory protein-1α and interleukin-1β increases in hypothyroidism. However, in Kupffer cells, proinflammatory activities such as the respiratory burst, nitric oxide synthase activity, and tumor necrosis factor-α expression may result from increased T(3) levels. Thyroid hormones also affect natural killer cell activity and cell-mediated immune responses. Still, for many immune cells no clear correlation has been found so far between abnormally high or low T(3) or T(4) levels and the effects observed on the immune responses. CONCLUSIONS: In this review we outline the contributions of thyroid hormones to different aspects of innate and adaptive immune responses. The relationship between thyroid hormones and immune cells is complex and T(3) and T(4) may modulate immune responses through both genomic and nongenomic mechanisms. Future studies of the molecular signaling mechanisms involved in this cross-talk between thyroid hormones and the immune system may support development of new strategies to improve clinical immune responses.

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Crossref · 10.1089/thy.2010.0429

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  • Thyroid hormones can bind to integrin αvβ3 to switch on a cascade of signaling events through MAPK, phospholipase C, proteinkinase Cα, ERK1/2, and/or hypoxia-inducible factor-1, leading to enhanced cytokine and growth factor action and angiogenesis.

    “Thyroid hormones can bind to the integrin αvβ3 to switch on a cascade of signaling events through MAPK, phospholipase C, proteinkinase Cα, ERK1/2, and/or hypoxia-inducible factor-1, leading to enhanced cytokine and growth factor action and angiogenesis [128].”
  • Thyroid hormones induce oxygen radical production in neutrophils, IFN-γ-stimulated major histocompatibility complex class II expression, IL-6, IL-8, and IL-12 secretion from different cell types, lymphocyte proliferation, IFN-γ-stimulated natural killer cell activity, and superoxide anion production in human alveolar neutrophils and macrophages.

    “Thyroid hormones induce oxygen radical production in neutrophils [128], IFN-γ-stimulated major histocompatibility complex class II expression [128], IL-6, IL-8, and IL-12 secretion from different cell types [128], lymphocyte proliferation [128], IFN-γ-stimulated natural killer cell activity [128], and superoxide anion production in human alveolar neutrophils and macrophages [129].”

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Authors
De Vito, P., Incerpi, S., Pedersen, J. Z., Luly, P., Davis, F. B., & Davis, P. J.
Affiliations
  • Department of Biology, University of Rome Tor Vergata, Rome, Italy.
  • Roma Tre University (IT)
  • University of Rome Tor Vergata (IT)
  • Signal Transduction Laboratory, Ordway Research Institute, Inc., Albany, New York.
Corresponding author
Incerpi, Sandra
Venue
Thyroid
Published
2011-08
Volume
21
Issue
8
Pages
879-890
ISSN
  • 1050-7256 (ISSN-L)
  • 1557-9077
OpenAlex
W2051241287
Cited by
347
References
163
Citations by year
2026: 16 · 2025: 24 · 2024: 22 · 2023: 34 · 2022: 44 · 2021: 31 · 2020: 30 · 2019: 29 · 2018: 15 · 2017: 26 · 2016: 18 · 2015: 18 · 2014: 15 · 2013: 15 · 2012: 10
FWCI
10.44
Type
journal article
Language
en
Open access
closed
Locations
  • Thyroid (publishedVersion)
  • PubMed (publishedVersion)
  • Cineca Institutional Research Information System (Tor Vergata University) (submittedVersion)
  • Iris (Roma Tre University) (submittedVersion)
Funders
U.S. Food and Drug Administration
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Disorders and Treatments
  • Life Sciences › Immunology and Microbiology › Immunology › Immunotoxicology and immune responses
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
Keywords
thyroid hormones, thyroxine, triiodothyronine, immunomodulation, hyperthyroidism, hypothyroidism, monocytes, macrophages, Kupffer cells, natural killer cells, phagocytosis, reactive oxygen species, cytokine production, macrophage inflammatory protein-1alpha, IL-1β, TNF-α, nitric oxide synthase, respiratory burst, innate immunity, adaptive immunity
MeSH terms
Animals, Humans, Hyperthyroidism, Immune System, Macrophages, Models, Biological, Thyroid Hormones, Thyroxine, Triiodothyronine, Reactive Oxygen Species, Interleukin-1beta, Chemokine CCL3

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