Th17 plasticity and its changes associated with inflammatory bowel disease

Area of Science:

• Immunology
• Cellular Biology
• Molecular Medicine

Background:

• CD4 T helper (Th) cell differentiation was traditionally viewed as a fixed process.
• Recent findings reveal T cell plasticity, where cells can adopt multiple functional phenotypes.
• This plasticity challenges the immutability of established T helper cell subsets.

Purpose of the Study:

• To review the evidence for T helper 17 (Th17) cell plasticity.
• To explore the underlying mechanisms governing Th17 cell plasticity.
• To highlight therapeutic strategies targeting Th17 plasticity in inflammatory bowel diseases (IBD).

Main Methods:

• Review of existing scientific literature on T cell differentiation and plasticity.
• Analysis of studies investigating T helper 17 (Th17) cell function and phenotypes.
• Examination of mechanisms driving transdifferentiation and cytokine/transcription factor co-expression.

Main Results:

• Evidence supports Th17 cell plasticity, with cells co-expressing markers of Th1 (interferon-γ) or regulatory T cells (forkhead box p3).
• Th17 cells can exhibit characteristics of multiple T helper subsets, indicating a dynamic functional state.
• This plasticity is implicated in the immune pathology of inflammatory bowel diseases.

Conclusions:

• T helper cell plasticity, particularly within the Th17 subset, is a significant feature of immune responses.
• Understanding the mechanisms of Th17 plasticity is crucial for comprehending immune dysregulation in IBD.
• Targeting Th17 plasticity offers a potential therapeutic avenue for managing human inflammatory bowel diseases.