Nasal Streptococcus pyogenes Infection Exacerbates Psoriasiform Relapse in Mice Through TLR2-Dependent Dendritic Cell
Lijiaming Zhou1,2, Zhengchun Wang1, Jingxia Zhao1
1Department of Dermatology, Beijing Hospital of Traditional Chinese Medicine, Capital Medical University, Beijing Institute of Traditional Chinese Medicine, Beijing, People's Republic of China.
Journal of Inflammation Research
|August 11, 2026
Summary
Nasal Streptococcus pyogenes infection worsens psoriasis by reprogramming dendritic cells. These cells migrate to the skin, promoting IL-17A production and disease relapse via TLR2 signaling.
Area of Science:
- Immunology
- Dermatology
- Metabolic pathways
Background:
- Nasal Streptococcus pyogenes (SP) infection is linked to psoriasis relapse.
- The immune mechanisms connecting systemic infection to cutaneous disease are not fully understood.
- Dendritic cell (DC) reprogramming and migration are investigated as key players.
Purpose of the Study:
- To elucidate the role of dendritic cell (DC) metabolic reprogramming and trafficking in SP-induced psoriasis relapse.
- To understand the systemic-to-cutaneous immune relay in psoriasis.
Main Methods:
- A murine psoriasis model was induced by imiquimod (IMQ) and intranasal SP challenge.
- Disease severity, immune cell infiltration, cytokine levels, and DC function (metabolism, migration) were assessed.
- RNA-sequencing, qPCR, Western blot, flow cytometry, and bioluminescence imaging were employed.
Main Results:
- Nasal SP infection aggravated psoriasis-like lesions, increasing PASI scores and IL-17A levels.
- SP induced DC aerobic glycolysis and hyper-mobility via TLR2/NF-κB/NOS2 signaling.
- DCs trafficked to the skin, forming synapses with γδ T cells to promote IL-17A production.
Conclusions:
- Nasal SP infection exacerbates psoriasis relapse through TLR2-dependent DC metabolic reprogramming and trafficking.
- This process promotes γδ T cell IL-17A production, driving disease.
- Further validation in human cohorts is needed for clinical translation.
