Impact of Helminth Infection on Th17 Cell Plasticity: Modulation of Inflammatory Responses and Enhancement of Regulatory Functions
By
Ahmed Metwali
Sarah Winckler
Xiaoqun Guan
M. Nedim Ince
David E. Elliott
April 28, 2026
Clinical Scorecard: Impact of Helminth Infection on Th17 Cell Plasticity: Modulation of Inflammatory Responses and Enhancement of Regulatory Functions
At a Glance
Category Detail
Condition Helminth Infection and Th17 Cell Plasticity (specifically Heligmosomoides polygyrus) Key Mechanisms Helminth infection alters Th17 cell behavior, promoting regulatory functions and inhibiting pathogenic inflammation, particularly through Heligmosomoides polygyrus. Target Population Individuals with autoimmune and inflammatory-mediated diseases, particularly those affected by Th17-driven pathology. Care Setting Research and clinical settings focusing on immune-mediated diseases, including autoimmune disorders.
Key Highlights
Helminth infection suppresses Th17 activity and reduces pathogenic inflammation. Th17 cells exhibit plasticity, transitioning to regulatory Tr1/Treg-like functions. Helminth exposure decreases the frequency of pathogenic Th17 cells in the immune system. The specific helminth studied is Heligmosomoides polygyrus. Guideline-Based Recommendations
Diagnosis
Assess Th17 cell activity in patients with autoimmune diseases. Management
Consider helminth therapy (specifically Heligmosomoides polygyrus) as a potential modulator of Th17 responses in autoimmune conditions. Monitoring & Follow-up
Monitor changes in Th17 cell populations and their functional profiles post-helminth exposure. Risks
Evaluate the risk of helminth infection in immunocompromised patients. Patient & Prescribing Data
Patients with autoimmune and inflammatory diseases.
Helminth therapy may enhance regulatory T cell functions and suppress inflammatory responses.
Clinical Best Practices
Incorporate helminth exposure (specifically Heligmosomoides polygyrus) in therapeutic strategies for managing autoimmune diseases. Utilize Th17 lineage reporter models for studying immune responses. References
