T helper 17 cells, commonly known as Th17 cells, are a subset of pro-inflammatory T helper cells defined by their production of interleukin 17 (IL-17). They play a crucial role in the immune system, particularly in the defense against extracellular bacteria and fungi, and are involved in the pathogenesis of various autoimmune diseases. Th17 cells are distinct from other T helper cell lineages (such as Th1 and Th2). They are generated from CD4+ T cells in response to specific cytokines. Key factors involved in Th17 differentiation include:

  • Transforming growth factor beta (TGF-β)
  • Interleukin 6 (IL-6)
  • Interleukin 21 (IL-21)
  • Interleukin 23 (IL-23)

These cytokines are produced by activated antigen-presenting cells (APCs) after encountering pathogens. The differentiation program of Th17 cells can lead to either protective or pro-inflammatory pathogenic cells. Interestingly, Th17 cells can also give rise to regulatory T h 17 (Treg17) cells, which have non-pathogenic roles and contribute to maintaining mucosal barriers.

Functions of Th17 cells

Th17 cells play a role in adaptive immunity by protecting the body against pathogens. Their main effector cytokines include IL-17A, IL-17F, IL-21, IL-22 and granulocyte-macrophage colony-stimulating factor (GM-CSF). IL-17 family cytokines target innate immune cells and epithelial cells, promoting neutrophil production and recruitment. Th17 cells regulate neutrophils, while Th1 cells regulate macrophages and monocytes, and Th2 cells regulate eosinophils, basophils, and mast cell. Th17 cells have a complex role in cancer. They can either promote or inhibit tumor growth depending on the context and the tumor microenvironment. In some cancers, Th17 cells contribute to anti-tumor immunity by recruiting immune cells to the tumor site, while in others, they may promote tumor growth and metastasis. IL-17 has been shown to play a role in bone metabolism. While it can contribute to bone destruction in inflammatory diseases like rheumatoid arthritis, it also participates in normal bone remodeling processes.

Dysregulated Th17 cell responses can contribute to the development of autoimmune diseases such as multiple sclerosis, rheumatoid arthritis, psoriasis, and inflammatory bowel disease (IBD). The chronic production of IL-17 and other cytokines can lead to tissue damage and sustained inflammation. Th17 cells often interact with other T cell subsets, such as regulatory T cells (Tregs), to maintain immune homeostasis. An imbalance between Th17 and Treg cells can contribute to autoimmunity and chronic inflammatory conditions.

Role of Th17 cells in pathogenesis of periodontal disease

Inflammation and immune response

Th17 cells play a significant role in the pathogenesis of periodontal diseases. As already stated, these cells secrete IL-17. IL-17, in particular, is a key player in periodontal inflammation. It promotes the production of other inflammatory mediators like IL-6, IL-8, and TNF-α by various cell types, including gingival fibroblasts, epithelial cells, and macrophages. Along with this, IL-17 is crucial for recruiting neutrophils to the site of infection. While neutrophils are essential for controlling bacterial infections, their excessive recruitment and activation can lead to tissue damage and bone resorption characteristic of periodontal diseases.


Th17 cell-derived IL-17 promotes the differentiation and activation of osteoclasts, the cells responsible for bone resorption. This process is mediated through the upregulation of receptor activator of nuclear factor-kappa B ligand (RANKL) on osteoblasts and stromal cells, which interacts with its receptor RANK on osteoclast precursors, leading to bone loss in periodontal disease. Th17 cells express high levels of RANKL (Receptor Activator of Nuclear Factor Kappa-B Ligand) on their surface.

Regulation of Th17 cell production

The production and differentiation of T helper (Th) cells are tightly regulated by a complex interplay of signals from the environment, including cytokines, antigen presentation, and interactions with other immune cells. This regulation ensures a balanced immune response to various pathogens and prevents inappropriate or excessive immune activity that could lead to autoimmune diseases or chronic inflammation. TGF-β, IL-6, IL-21, and IL-23 are key cytokines for Th17 differentiation. Th17 cell production is regulated by multiple mechanisms. The feedback mechanism is one of them. Each Th cell subset can produce cytokines that inhibit the differentiation of other subsets. For example, IFN-γ produced by Th1 cells can inhibit Th2 and Th17 differentiation, while IL-4 from Th2 cells can inhibit Th1 differentiation. T-regulator cells also regulate the production of Th17 cells. Tregs help maintain immune homeostasis by suppressing the activation and differentiation of other Th cells through the production of anti-inflammatory cytokines like IL-10 and TGF-β.


Understanding the role of Th17 cells in immune responses and their involvement in diseases provides insight into potential therapeutic targets for modulating immune function. Th17 cells also contribute to bone resorption by promoting osteoclast differentiation, while Treg cells play a protective role. The production and differentiation of Th cells are regulated by a combination of antigen presentation, cytokine signals, transcription factors, signal transduction pathways, microenvironmental factors, regulatory mechanisms, and epigenetic changes.

Periobasics: A Textbook of Periodontics and Implantology

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