The interplay of thyroid hormones and the immune system – where we stand and why we need to know about it

Wenzek, Christina; Boelen, Anita; Westendorf, Astrid M.; Engel, Daniel R.; Moeller, Lars C.; Führer, Dagmar

doi:10.1530/eje-21-1171

Cited by 53 publications

(40 citation statements)

References 117 publications

(185 reference statements)

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“…On the one hand, autoimmune‐related pathologies can affect this balance. On the other hand, THs regulate innate and adaptive immune responses, as immune cells are the direct target cells of THs 35–37 . In patients with GD, we found for the first time that overexpression of BAFF caused abnormal differentiation of ASCs and was positively correlated with FT3, FT4, and TRAb levels.…”

Section: Discussionmentioning

confidence: 77%

“…On the other hand, THs regulate innate and adaptive immune responses, as immune cells are the direct target cells of THs. [35][36][37] In patients with GD, we found for the first time that overexpression of BAFF caused abnormal differentiation of ASCs and was positively correlated with FT3, FT4, and TRAb levels. In addition, the fact that BAFF overexpression is also present in the GHNR group needs to be elucidated, which may explain the initial development of GD, due to TRAb being the cause of GH.…”

Section: Discussionmentioning

confidence: 80%

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High levels of thyroid hormones promote recurrence of Graves' disease via overexpression of B‐cell‐activating factor

Liu

Miao

Zhou

et al. 2022

Clinical Laboratory Analysis

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Background Elevated thyroid hormone (TH) levels have been suggested to be associated with the pathological progression of Graves' disease (GD). However, direct evidence from clinical studies remains unclear. Methods Peripheral blood samples were collected from patients with or without the recurrence of Graves' hyperthyroidism (GH) and healthy donors. Thyroid tissue samples were obtained from patients with benign thyroid nodules. To assess the differentiation of autoreactive B cells, the expression of B‐cell‐activating factor (BAFF) and the proportion of CD11c+/–IgG+/− subsets of B cells stimulated by high levels of triiodothyronine (T3) in vivo and in vitro were examined by ELISA, flow cytometry, western blotting, and qRT‐PCR. Results Serum BAFF levels in patients with GD were significantly and positively correlated with FT3, FT4, and TRAb levels. Furthermore, the ratio of abnormally differentiated CD11c+ autoreactive B cells positively correlated with BAFF and TRAb. High levels of triiodothyronine (T3) induced BAFF overexpression in thyroid follicular cells and mononuclear cells of the normal thyroid in vitro, thereby promoting the differentiation of CD11c+IgG+ autoreactive secretory B cells (ASCs). However, the precise knockdown of BAFF expression significantly inhibited the abnormal differentiation of ASCs. Conclusion The pathological progression of GD was prolonged and exacerbated by autoimmune positive feedback modulation caused by high TH levels. BAFF could be considered a potential target for localized thyroid immunosuppressive treatment of Graves' hyperthyroidism recurrence.

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Section: Discussionmentioning

confidence: 77%

Section: Discussionmentioning

confidence: 80%

High levels of thyroid hormones promote recurrence of Graves' disease via overexpression of B‐cell‐activating factor

Liu

Miao

Zhou

et al. 2022

Clinical Laboratory Analysis

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“…In order to understand how pre-vaccination transcriptional state is associated with post-vaccination antibody response, we performed a DE analysis of high-vs. low-responders in the pre-vaccination state, and identified 12 up-regulated and 7 down-regulated RNAs in high responders; up-regulated RNAs included THRB, BLZF1, MPIG6B , and CCR1 (Supplementary Table 7). The expression of THRB , a nuclear receptor for thyroid hormone, is intriguing in view of the reported role of thyroid hormone on immune response, particularly in the innate immune system 24,25 . The association of MPIG6B with vaccine response is notable since it acts as a platelet inhibitory receptor that has also been implicated in early megakaryocyte development 26,27 .…”

Section: Resultsmentioning

confidence: 99%

Platelet response to influenza vaccination reflects effects of aging

Konstorum

Mohanty

Zhao

et al. 2022

Preprint

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Platelets are uniquely positioned as mediators of not only hemostasis but also innate immunity, but how age and alterations in functional status such as frailty influence platelet function during an immune response remains unclear. We assessed the platelet transcriptome in younger (age 21-35) and older (age ≥ 65) adults (including frail and non-frail individuals) following influenza vaccination. Prior to vaccination, we identified an age- and frailty-associated increase in expression of platelet activation and mitochondrial RNAs and decrease in RNAs encoding proteins mediating translation. Using tensor decomposition analysis, we also elucidated dynamic post-vaccination platelet activation and translation signatures associated with age and frailty. At the protein level, enhanced platelet activation was found in non-frail older adults, compared to young individuals both prior to and post-vaccine; but frail adults showed decreased platelet activation compared to non-frail that could reflect the influence of decreased translation RNA expression. Our results reveal an age-dependent alteration in platelet function prior to and post-vaccination that may contribute to age-associated chronic inflammation.

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“…TSH/TSH-R have been proposed to influence immune regulation ( 32 ). TSH-R expression was found in bone marrow hematopoietic cells, where TSH may regulate TNFα production ( 33 ).…”

Section: Tsh Receptor Expressionmentioning

confidence: 99%

“…In white blood cells, TSH-R may be involved in recruitment, development and immunoregulation ( 23 ). This receptor has been found to be expressed on monocytes, dendritic cells, natural killer cells, T and B cells ( 32 ). Stimulation with recombinant human TSH has been shown to promote proliferation of natural killer cells, T and B cells ( 35 ).…”

Section: Tsh Receptor Expressionmentioning

confidence: 99%

The Mysterious Universe of the TSH Receptor

2022

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The thyroid-stimulating hormone receptor (TSH-R) is predominantly expressed in the basolateral membrane of thyrocytes, where it stimulates almost every aspect of their metabolism. Several extrathyroidal locations of the receptor have been found including: the pituitary, the hypothalamus, and other areas of the central nervous system; the periorbital tissue; the skin; the kidney; the adrenal; the liver; the immune system cells; blood cells and vascular tissues; the adipose tissue; the cardiac and skeletal muscles, and the bone. Although the functionality of the receptor has been demonstrated in most of these tissues, its physiological importance is still a matter of debate. A contribution to several pathological processes is evident in some cases, as is the case of Grave’s disease in its multiple presentations. Conversely, in the context of other thyroid abnormalities, the contribution of the TSH-R and its ligand is still a matter of debate. This article reviews the several different sites of expression of the TSH-R and its potential role in both physiological and pathological processes.

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The interplay of thyroid hormones and the immune system – where we stand and why we need to know about it

Cited by 53 publications

References 117 publications

High levels of thyroid hormones promote recurrence of Graves' disease via overexpression of B‐cell‐activating factor

High levels of thyroid hormones promote recurrence of Graves' disease via overexpression of B‐cell‐activating factor

Platelet response to influenza vaccination reflects effects of aging

The Mysterious Universe of the TSH Receptor

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