Tissue Infiltrating LTi—Like Group 3 Innate Lymphoid Cells and T Follicular Helper Cells in Graves' and Hashimoto's Thyroiditis

Mohr, Audrey; Trésallet, Christophe; Monot, Natacha; Bauvois, Adeline; Abiven, Delphine; Atif, Muhammad; Claër, Laetitia; Malhotra, Rajneesh; Mayer, Gaëll; Balderas, Robert; Vaarala, Outi; Deniziaut, Gabrielle; Brochériou, Isabelle; Buffet, C; Leenhardt, Laurence; Gorochov, Guy; Miyara, Makoto

doi:10.3389/fimmu.2020.00601

Cited by 13 publications

(11 citation statements)

References 36 publications

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“…[ 30 ] It has also been reported that the positive rate of TG-Ab in patients with HT is 25% to 50%, whereas that of TPO-Ab is 90%. [ 31 ] In this study, we found that TG-Ab and TPO-Ab were both higher in patients with MN and HT or GD than in those with MN alone. Furthermore, we found that the expression of TPO-Ab in renal tissues was more prevalent in patients with MN and AITD than in those with MN alone.…”

Section: Discussionmentioning

confidence: 51%

Relationship between autoimmune thyroid disease and nephropathy

Zhao

Liu

et al. 2021

Medicine

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The association of nephropathy with autoimmune thyroid disease (AITD) has been reported previously. However, there is limited information on the relationship between thyroid autoantibodies and nephropathy. A retrospective study was conducted using the medical records of 246 patients with nephropathy, 82 of whom had concurrent AITD. General characteristics, thyroid function, autoantibodies, and the pathological types of nephropathy were analyzed. Immunohistochemistry was used to detect the thyroglobulin antibody (TG-Ab) and thyroid peroxidase antibody (TPO-Ab) in the kidneys. We found nephropathy patients with AITD exhibited higher serum levels of TPO-Ab, TG-Ab, thyroid-stimulating hormone receptor antibody (TR-Ab), and immunoglobulin G (IgG) ( P < .05). Compared with the nephropathy without AITD group, the nephropathy with AITD group exhibited higher proportions of membranous nephropathy (MN) and focal segmental glomerulosclerosis (FSGS), and relatively lower proportions of mesangial proliferative glomerulonephritis (MsPGN) and minimal change nephropathy (MCN) ( P = .005). TPO-Ab and TG-Ab levels in the kidney were more prevalent in nephropathy patients with AITD than those without AITD ( P = .015 and P = .026, respectively). Subgroup analysis demonstrated that serum levels of thyroid stimulating hormone (TSH), TG-Ab, TPO-Ab, immunoglobulin M (IgM), and IgG in the MN group were significantly higher, whereas the levels of free thyroxine (FT4) and estimated glomerular filtration rate (eGFR) were lower, as compared with MN with Hashimoto thyroiditis (HT) group ( P < .05). TPO-Ab and TG-Ab expression levels in the kidneys were more prevalent in the MN group than in the MN with HT group ( P = .034). The expression levels of FT4, TG-Ab, TPO-Ab, and thyroid-stimulating hormone receptor antibody (TSHR-Ab) in the serum were significantly higher in the MN group than in the MN with Graves disease (GD) group ( P < .05). The expression of TPO-Ab in the kidneys was more prevalent in the MN group than in the MN with GD group ( P = .011). In sum, the expressions of TPO-Ab and TG-Ab were more prevalent in the kidneys of patients with nephropathy and AITD. Our findings indicate that TPO-Ab and TG-Ab may play a role in the development of AITD-related nephropathy.

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Section: Discussionmentioning

confidence: 51%

Relationship between autoimmune thyroid disease and nephropathy

Zhao

Liu

et al. 2021

Medicine

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“…All mentioned findings indicate that the transition from prediabetes to diabetes in NOD mice is associated with impaired ILC3 function that could lead to reduced numbers of Treg and imply the protective role of IL-2 + and IL-22 + ILC3 against T1D. In general, there are many pathological conditions where ILC3 play a role such as inflammatory bowel disease, experimental autoimmune encephalomyelitis, Graves’ and Hashimoto’s thyroiditis ( 52 , 80 – 82 ). Still, further investigation will discriminate whether ILC3 reduction precedes or is the result of ongoing inflammation during T1D pathogenesis.…”

Section: Ilc3 In T1dmentioning

confidence: 99%

Modulation of Intestinal ILC3 for the Treatment of Type 1 Diabetes

et al. 2021

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Gut-associated lymphoid tissue (GALT) is crucial for the maintenance of the intestinal homeostasis, but it is also the potential site of the activation of autoreactive cells and initiation/propagation of autoimmune diseases in the gut and in the distant organs. Type 3 innate lymphoid cells (ILC3) residing in the GALT integrate signals from food ingredients and gut microbiota metabolites in order to control local immunoreactivity. Notably, ILC3 secrete IL-17 and GM-CSF that activate immune cells in combating potentially pathogenic microorganisms. ILC3 also produce IL-22 that potentiates the strength and integrity of epithelial tight junctions, production of mucus and antimicrobial peptides thus enabling the proper function of the intestinal barrier. The newly discovered function of small intestine ILC3 is the secretion of IL-2 and the promotion of regulatory T cell (Treg) generation and function. Since the intestinal barrier dysfunction, together with the reduction in small intestine ILC3 and Treg numbers are associated with the pathogenesis of type 1 diabetes (T1D), the focus of this article is intestinal ILC3 modulation for the therapy of T1D. Of particular interest is free fatty acids receptor 2 (FFAR2), predominantly expressed on intestinal ILC3, that can be stimulated by available selective synthetic agonists. Thus, we propose that FFAR2-based interventions by boosting ILC3 beneficial functions may attenuate autoimmune response against pancreatic β cells during T1D. Also, it is our opinion that treatments based on ILC3 stimulation by functional foods can be used as prophylaxis in individuals that are genetically predisposed to develop T1D.

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“…Another population, called T regulatory cells (Tregs), crucial for maintaining T-cell tolerance to self-antigens, is dysfunctional in autoimmune thyroiditis as recently demonstrated [ 91 , 92 ].…”

Section: Adaptive and Innate Immune Response Surrounding Ptc In The C...mentioning

confidence: 99%

The Immune Landscape of Papillary Thyroid Cancer in the Context of Autoimmune Thyroiditis

Pani

Caria

Yasuda

et al. 2022

Cancers

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Papillary thyroid cancer (PTC) often co-occurs with Hashimoto’s thyroiditis, an association that has long been reported in clinical studies, remaining controversial. Experimental evidence has recently shown that pre-existing thyroiditis has a beneficial effect on PTC growth and progression by a distinctive expansion of effector memory CD8 T cells. Although the link between inflammation and PTC might involve different components of the immune system, a deep characterization of them which includes T cells, B cells and tertiary lymphoid structures, Mye-loid cells, Neutrophils, NK cells and dendritic cells will be desirable. The present review article considers the role of the adaptive and innate immune response surrounding PTC in the context of Hashimoto’s thyroiditis. This review will focus on the current knowledge by in vivo and in vitro studies specifically performed on animals’ models; thyroid cancer cells and human samples including (i) the dual role of tumor-infiltrating lymphocytes; (ii) the emerging role of B cells and tertiary lymphoid structures; (iii) the role of myeloid cells, dendritic cells, and natural killer cells; (iv) the current knowledge of the molecular biomarkers implicated in the complex link between thyroiditis and PTC and the potential implication of cancer immunotherapy in PTC patients in the context of thyroiditis.

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Tissue Infiltrating LTi—Like Group 3 Innate Lymphoid Cells and T Follicular Helper Cells in Graves' and Hashimoto's Thyroiditis

Cited by 13 publications

References 36 publications

Relationship between autoimmune thyroid disease and nephropathy

Relationship between autoimmune thyroid disease and nephropathy

Modulation of Intestinal ILC3 for the Treatment of Type 1 Diabetes

The Immune Landscape of Papillary Thyroid Cancer in the Context of Autoimmune Thyroiditis

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