# Immunopathogenesis, Diagnosis, and Treatment of Hashimoto’s Thyroiditis

**Authors:** Felicia Delgadillo, Devendra K. Agrawal

PMC · DOI: 10.26502/aimr.0232 · Archives of internal medicine research · 2026-02-19

## TL;DR

This paper reviews the immune causes, diagnosis, and treatment of Hashimoto’s thyroiditis, an autoimmune thyroid disorder.

## Contribution

The paper highlights recent insights into Th17 cells and oxidative stress in Hashimoto’s thyroiditis pathogenesis.

## Key findings

- Hashimoto’s thyroiditis involves Th1, Th17, and regulatory T cell imbalances.
- Levothyroxine is the main treatment, with vitamin D and selenium as emerging adjuncts.
- Personalized therapies targeting autoimmunity are needed for better patient outcomes.

## Abstract

This comprehensive literature review examines the immunopathogenesis of Hashimoto’s thyroiditis, a prevalent autoimmune thyroid disorder. Hashimoto’s thyroiditis results from a complex interplay of genetic predisposition and environmental triggers, leading to loss of immune tolerance to thyroid antigens. Hashimoto’s thyroiditis involves both cellular (T cells) and humoral (B cells, autoantibodies) responses. Key players include Th1, Th17, and regulatory T cells, with an imbalance in the Th17/Treg ratio implicated. The diagnosis of Hashimoto’s thyroiditis relies on clinical presentation, thyroid function tests, detection of anti-thyroid peroxidase and anti-thyroglobulin antibodies, and ultrasound imaging. Current treatment of Hashimoto’s thyroiditis primarily involves levothyroxine replacement therapy. Emerging adjunctive approaches include vitamin D and selenium supplementation. Some potential challenges of Hashimoto’s thyroiditis include understanding precise disease triggers, developing predictive biomarkers, and addressing persistent symptoms despite biochemical euthyroid. This article highlights recent advances in understanding the pathogenesis of Hashimoto’s thyroiditis, particularly the roles of Th17 cells and oxidative stress. It also discusses controversies and knowledge gaps, such as the exact mechanisms that initiate autoimmunity and the factors that influence disease progression. There is a need for personalized treatment strategies and therapies targeting the underlying autoimmune process for better treatment of patients with Hashimoto’s Thyroiditis.

## Linked entities

- **Chemicals:** levothyroxine (PubChem CID 5819), selenium (PubChem CID 6326970)
- **Diseases:** Hashimoto’s thyroiditis (MONDO:0007699)

## Full-text entities

- **Genes:** IL2 (interleukin 2) [NCBI Gene 3558] {aka IL-2, TCGF, lymphokine}, TPO (thyroid peroxidase) [NCBI Gene 7173] {aka MSA, TDH2A, TPX}, CD4 (CD4 molecule) [NCBI Gene 920] {aka CD4mut, IMD79, Leu-3, OKT4D, T4}, IL12B (interleukin 12B) [NCBI Gene 3593] {aka CLMF, CLMF2, IL-12B, IMD28, IMD29, NKSF}, FOXP3 (forkhead box P3) [NCBI Gene 50943] {aka AIID, DIETER, IPEX, JM2, PIDX, XPID}, IL21 (interleukin 21) [NCBI Gene 59067] {aka CVID11, IL-21, Za11}, HLA-A (major histocompatibility complex, class I, A) [NCBI Gene 3105] {aka HLAA}, TSHR (thyroid stimulating hormone receptor) [NCBI Gene 7253] {aka CHNG1, LGR3, hTSHR-I}, PTPN22 (protein tyrosine phosphatase non-receptor type 22) [NCBI Gene 26191] {aka LYP, LYP1, LYP2, PEP, PTPN22.5, PTPN22.6}, IL18 (interleukin 18) [NCBI Gene 3606] {aka IGIF, IL-18, IL-1g, IL1F4}, TGM2 (transglutaminase 2) [NCBI Gene 7052] {aka G(h), TG(C), TGC, hTG2, tTG}, IFNG (interferon gamma) [NCBI Gene 3458] {aka IFG, IFI, IMD69}, CTLA4 (cytotoxic T-lymphocyte associated protein 4) [NCBI Gene 1493] {aka ALPS5, CD, CD152, CELIAC3, CTLA-4, GRD4}, SLC5A5 (solute carrier family 5 member 5) [NCBI Gene 6528] {aka NIS, TDH1}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, IL10 (interleukin 10) [NCBI Gene 3586] {aka CSIF, GVHDS, IL-10, IL10A, TGIF}, BACH2 (BACH transcriptional regulator 2) [NCBI Gene 60468] {aka BTBD25, IMD60}, IL23A (interleukin 23 subunit alpha) [NCBI Gene 51561] {aka IL-23, IL-23A, IL23P19, P19, SGRF}, TG (thyroglobulin) [NCBI Gene 7038] {aka AITD3, TGN}, IL17A (interleukin 17A) [NCBI Gene 3605] {aka CTLA-8, CTLA8, IL-17, IL-17A, IL17, ILA17}, CXCL10 (C-X-C motif chemokine ligand 10) [NCBI Gene 3627] {aka C7, IFI10, INP10, IP-10, SCYB10, crg-2}, SELENOS (selenoprotein S) [NCBI Gene 55829] {aka AD-015, ADO15, SBBI8, SELS, SEPS1, VIMP}, IL22 (interleukin 22) [NCBI Gene 50616] {aka IL-21, IL-22, IL-D110, IL-TIF, ILTIF, TIFIL-23}, FASLG (Fas ligand) [NCBI Gene 356] {aka ALPS1B, APT1LG1, APTL, CD178, CD95-L, CD95L}, IL1B (interleukin 1 beta) [NCBI Gene 3553] {aka IL-1, IL1-BETA, IL1F2, IL1beta}, FAS (Fas cell surface death receptor) [NCBI Gene 355] {aka ALPS1A, APO-1, APT1, CD95, FAS1, FASTM}, HLA-C (major histocompatibility complex, class I, C) [NCBI Gene 3107] {aka D6S204, HLA-JY3, HLAC, HLC-C, MHC, PSORS1}, CD8A (CD8 subunit alpha) [NCBI Gene 925] {aka CD8, CD8alpha, IMD116, Leu2, p32}
- **Diseases:** fatigue (MESH:D005221), PTC (MESH:D000077273), type 1 diabetes (MESH:D003922), constipation (MESH:D003248), Vitamin D deficiency (MESH:D014808), hyperthyroidism (MESH:D006980), Proinflammatory cytokines (MESH:D000080424), thyroid lymphoma (MESH:D008223), AITD (MESH:D013967), thyroid conditions (MESH:D013959), weight gain (MESH:D015430), autoimmune (MESH:D001327), congenital rubella (MESH:D012410), musculoskeletal pain (MESH:D059352), Infiltration (MESH:D017254), cognitive impairment (MESH:D003072), Graves' disease (MESH:D006111), Hashimoto (MESH:D050031), celiac disease (MESH:D002446), autoimmune diathesis (MESH:D004198), cysts (MESH:D003560), neurological dysfunction (MESH:D009461), multiple sclerosis (MESH:D009103), seizures (MESH:D012640), impaired thyroid function (MESH:D013966), autoimmune destruction (MESH:D008105), goiter (MESH:D006042), pernicious anemia (MESH:D000752), subacute thyroiditis (MESH:D013968), thyroid cancer (MESH:D013964), thyroid nodules (MESH:D016606), Hypothyroidism (MESH:D007037), micronutrient deficiencies (MESH:D007153), Complications (MESH:D008107), autoimmune inflammation (MESH:D007249), fibrosis (MESH:D005355), postpartum thyroiditis (MESH:D050032), dry skin (MESH:D015352), cytotoxicity (MESH:D064420), neurological complications (MESH:D002493), Hashimoto's encephalopathy (MESH:C535841), hepatitis C (MESH:D019698), atrophy (MESH:D001284), cold intolerance (MESH:D000067390), psychiatric symptoms (MESH:D001523), thyroid-associated orbitopathy (MESH:D049970), Infections (MESH:D007239), immune dysfunction (MESH:D007154), Euthyroidism (MESH:D005067), malignancy (MESH:D009369)
- **Chemicals:** lithium (MESH:D008094), iron (MESH:D007501), Iodine (MESH:D007455), steroid (MESH:D013256), iodide (MESH:D007454), Mg (MESH:D008274), calcium (MESH:D002118), ROS (MESH:D017382), alcohol (MESH:D000438), T3 (MESH:D014284), alkaloid (MESH:D000470), Zn (MESH:D015032), fT3 (-), L-T4 (MESH:D013974), Anatabine (MESH:C012737), Vitamin D (MESH:D014807), Se (MESH:D012643), Radioiodine (MESH:C000614965)
- **Species:** Nicotiana tabacum (American tobacco, species) [taxon 4097], Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12915989/full.md

## References

72 references — full list in the complete paper: https://tomesphere.com/paper/PMC12915989/full.md

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Source: https://tomesphere.com/paper/PMC12915989