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Related Concept Videos

T Cell Types and Functions01:24

T Cell Types and Functions

When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...

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Related Experiment Video

Updated: Jun 22, 2026

Rapid Isolation of BMPR-IB+ Adipose-Derived Stromal Cells for Use in a Calvarial Defect Healing Model
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γδ17T Cells Hinder Mandibular Bone Defect Healing.

R Naamneh1, F L Shoukair1, M Gera1

  • 1Institute of Biomedical and Oral Research, Faculty of Dental Medicine, Hebrew University, Jerusalem, Israel.

Journal of Dental Research
|December 17, 2025
PubMed
Summary
This summary is machine-generated.

Gamma delta T (γδT) cells and IL-17 delay mandibular fracture healing by prolonging inflammation. Depleting these cells or IL-17 accelerates bone repair, offering new therapeutic targets for jaw fractures.

Keywords:
IL-17drill holeflat boneinflammation, oral mucosa, fracture repair

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Area of Science:

  • Immunology
  • Skeletal Biology
  • Regenerative Medicine

Background:

  • Bone fracture healing involves complex immune-skeletal interactions, with flat bones like the mandible presenting unique challenges.
  • Mandibular fractures are common, complicated by oral microbiota and mechanical forces, impacting healing.
  • The role of interleukin-17 (IL-17) and γδT cells in bone repair remains controversial.

Purpose of the Study:

  • To investigate the role of IL-17-producing γδT cells (γδ17T cells) in mandibular defect healing.
  • To determine if targeting γδ17T cells or IL-17 can enhance mandibular bone regeneration.

Main Methods:

  • A murine model of mandibular drill hole defect was established for spontaneous healing studies.
  • γδT cell depletion (Tcrd-GDL mice) and IL-17 genetic ablation (Il17af-/- mice) were employed.
  • Leukocyte infiltration, RNA sequencing, and immunologic analyses were performed to assess healing kinetics and inflammatory responses.

Main Results:

  • Mandibular defects healed within 3 weeks, with distinct leukocyte infiltration patterns over time.
  • Depletion of γδT cells or IL-17 significantly accelerated mandibular healing kinetics.
  • IL-17 deficiency reduced later inflammatory responses without affecting early neutrophil and monocyte recruitment, leading to faster repair.

Conclusions:

  • IL-17-producing γδT cells delay mandibular fracture repair by hindering inflammation resolution.
  • Targeting γδ17T cells or IL-17 presents a potential therapeutic strategy to improve bone regeneration in mandibular fractures.