Immune cell summons
CXCL10 T-cell chemotaxis↓
Also searched as CXCL10 T-cell chemotaxis.
An engineered decoy of this signal improved survival and heart structure — and the authors were explicit that it worked without killing more virus. That is the clearest sign that at a certain stage it is the immune response, not the infection, doing the damage.
In depth
The signal that calls damaging T cells into the heart.
What drives it
Heart muscle inflammation 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.
What it drives
It increases Heart muscle inflammation.
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.
It increases Th17 immune arm.
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
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.