Th17 immune arm
IL-17-producing T helper cells↓
Also searched as IL-17-producing T helper cells.
Of all the immune cells involved, this one keeps turning up. Agents that help in this disease reduce its numbers and the signal it releases. It is pushed down this road by one cytokine and shouts another when it arrives — which is why both appear on this chain.
In depth
The immune cell type most consistently reduced when a treatment works in this illness.
What drives it
Heart muscle inflammation increases it.
The T cell that does the damage in this illness. Of all the immune cell types, this one keeps appearing when a treatment works: myricetin 'significantly decreased the percentage of Th17 cells in spleen and plasma IL-17A level' (doi 10.1016/j.ejphar.2023.175551 — Myricetin ameliorates experimental autoimmune myocarditis in mice by modulating immune response and inhibiting MCP-1 expression), and emodin works on the same axis in the viral model. IL-12 pushes cells down this road; IL-17 is what they release when they arrive. It is the most consistently targeted step in the whole disease. doi 10.1016/j.ejphar.2023.175551
Immune signaling increases it.
The T cell that does the damage in this illness. Of all the immune cell types, this one keeps appearing when a treatment works: myricetin 'significantly decreased the percentage of Th17 cells in spleen and plasma IL-17A level' (doi 10.1016/j.ejphar.2023.175551 — Myricetin ameliorates experimental autoimmune myocarditis in mice by modulating immune response and inhibiting MCP-1 expression), and emodin works on the same axis in the viral model. IL-12 pushes cells down this road; IL-17 is what they release when they arrive. It is the most consistently targeted step in the whole disease. doi 10.1016/j.ejphar.2023.175551
Immune cell summons increases it.
The summons that calls t cells into the heart — and blocking it saved lives without touching the virus. An engineered decoy version 'had significantly reduced heart/body weight ratio and serum CK-MB level, increased survival rate and improved heart histopathology'. And the mechanism is explicit: 'this therapeutic effect was not attributable to an enhanced viral clearance, but to a blunted Th1 immune response' (pmc3062568 — Direct Gene Transfer with ip-10 Mutant Ameliorates Mouse cvb3-Induced Myocarditis by Blunting Th1 Immune Responses). ⇒ you can save the heart without killing more virus. the immune response, not the infection, is doing the damage at this stage. REFUTED ON A SECOND READING. This link was shown by linked steps until a source was opened that does not support it: “Compared with vector or no treatment, pIP-10-AT treatment had significantly reduced heart/body weight ratio and serum CK-MB level, increased survival rate and improved heart histopathology, suggesting an ameliorated myocarditis. This therapeutic effect was not attributable to an enhanced viral clearance, but to a blunted Th1 immune response, as evidenced by significantly decreased splenic CD4+/CD8+IFN-γ+ T cell percentages and reduced myocardial Th1 cytokine levels.” — Direct Gene Transfer with IP-10 Mutant Ameliorates Mouse CVB3-Induced Myocarditis by Blunting Th1 Immune Responses. [journal/year/volume/pages NOT READ]. doi 10.1371/journal.pone.0018186
What it drives
It increases Inflammatory signaling.
The T cell that does the damage in this illness. Of all the immune cell types, this one keeps appearing when a treatment works: myricetin 'significantly decreased the percentage of Th17 cells in spleen and plasma IL-17A level' (doi 10.1016/j.ejphar.2023.175551 — Myricetin ameliorates experimental autoimmune myocarditis in mice by modulating immune response and inhibiting MCP-1 expression), and emodin works on the same axis in the viral model. IL-12 pushes cells down this road; IL-17 is what they release when they arrive. It is the most consistently targeted step in the whole disease. doi 10.1016/j.ejphar.2023.175551
It reduces Heart muscle cell.
The T cell that does the damage in this illness. Of all the immune cell types, this one keeps appearing when a treatment works: myricetin 'significantly decreased the percentage of Th17 cells in spleen and plasma IL-17A level' (doi 10.1016/j.ejphar.2023.175551 — Myricetin ameliorates experimental autoimmune myocarditis in mice by modulating immune response and inhibiting MCP-1 expression), and emodin works on the same axis in the viral model. IL-12 pushes cells down this road; IL-17 is what they release when they arrive. It is the most consistently targeted step in the whole disease. doi 10.1016/j.ejphar.2023.175551
Blends that modulate it
Each blend page names this pathway and carries the study behind its claim.
See it on the map
Open the causal map to follow this pathway upstream and downstream, arrow by arrow, each with its study.