Studies on innate immune receptors during GVHD
| PRR/species . | Observation . | Reference no. . |
|---|---|---|
| TLR4 | ||
| Human | TLR4 polymorphisms on patient and donor side cause more severe GVHD | 53 |
| Human | TLR4 polymorphisms do not cause more severe GVHD | 52 |
| Mouse | LPS antagonism results in less lethal GVHD | 27 |
| Mouse | LPS antagonism protects against lung injury after allo-BMT | 48 |
| TLR7 | ||
| Mouse | TLR7 agonism controls trafficking of T cells to GVHD target organs | 54 |
| TLR7/TLR8 | ||
| Mouse | TLR7/8 agonism after allo-BMT increases GVHD | 55 |
| Mouse | TLR7/8 agonism before allo-BMT ameliorates GVHD | 56 |
| TLR9 | ||
| Mouse | TLR9 agonism increases GVHD | 55 |
| Mouse | Lethal GVHD is reduced in TLR9−/− allo-BM transplant recipients | 50 |
| NOD2 | ||
| Human | NOD2 polymorphisms on patient and donor side cause more severe GVHD | 75 |
| Human | NOD2 polymorphisms on patient and donor side cause more severe GVHD | 76 |
| Human | NOD2 polymorphisms on patient and donor side cause more severe GVHD in recipients of a T cell–depleted HSC transplant | 79 |
| Human | NOD2 polymorphisms on patient and donor side cause more severe GVHD; Incidence of GVHD is reduced when NOD2 polymorphisms are on the donor side | 53 |
| Human | Increased pulmonary complications and death in patients with NOD2 polymorphisms after allo-HSCT. No significant difference in GVHD | 80 |
| Human | GVHD is not significantly increased in patients with NOD2 polymorphisms | 81 |
| Human | GVHD is not significantly increased in patients with NOD2 polymorphisms; Leukemia relapse rate is increased after allo-HSCT in patients with NOD2 polymorphisms | 82 |
| Human | GVHD is not significantly increased in children with NOD2 polymorphisms | 83 |
| Human | NOD2 polymorphisms in allo-HSC transplant recipients with GVHD are associated with diminished recruitment of CD4+ T cells and neutrophils in intestinal biopsies | 86 |
| Mouse | Lethal GVHD is increased in NOD2−/− allo-BM transplant recipients; NOD2 negatively regulates antigen-presenting cell (APC) function during GVHD | 65 |
| PRR/species . | Observation . | Reference no. . |
|---|---|---|
| TLR4 | ||
| Human | TLR4 polymorphisms on patient and donor side cause more severe GVHD | 53 |
| Human | TLR4 polymorphisms do not cause more severe GVHD | 52 |
| Mouse | LPS antagonism results in less lethal GVHD | 27 |
| Mouse | LPS antagonism protects against lung injury after allo-BMT | 48 |
| TLR7 | ||
| Mouse | TLR7 agonism controls trafficking of T cells to GVHD target organs | 54 |
| TLR7/TLR8 | ||
| Mouse | TLR7/8 agonism after allo-BMT increases GVHD | 55 |
| Mouse | TLR7/8 agonism before allo-BMT ameliorates GVHD | 56 |
| TLR9 | ||
| Mouse | TLR9 agonism increases GVHD | 55 |
| Mouse | Lethal GVHD is reduced in TLR9−/− allo-BM transplant recipients | 50 |
| NOD2 | ||
| Human | NOD2 polymorphisms on patient and donor side cause more severe GVHD | 75 |
| Human | NOD2 polymorphisms on patient and donor side cause more severe GVHD | 76 |
| Human | NOD2 polymorphisms on patient and donor side cause more severe GVHD in recipients of a T cell–depleted HSC transplant | 79 |
| Human | NOD2 polymorphisms on patient and donor side cause more severe GVHD; Incidence of GVHD is reduced when NOD2 polymorphisms are on the donor side | 53 |
| Human | Increased pulmonary complications and death in patients with NOD2 polymorphisms after allo-HSCT. No significant difference in GVHD | 80 |
| Human | GVHD is not significantly increased in patients with NOD2 polymorphisms | 81 |
| Human | GVHD is not significantly increased in patients with NOD2 polymorphisms; Leukemia relapse rate is increased after allo-HSCT in patients with NOD2 polymorphisms | 82 |
| Human | GVHD is not significantly increased in children with NOD2 polymorphisms | 83 |
| Human | NOD2 polymorphisms in allo-HSC transplant recipients with GVHD are associated with diminished recruitment of CD4+ T cells and neutrophils in intestinal biopsies | 86 |
| Mouse | Lethal GVHD is increased in NOD2−/− allo-BM transplant recipients; NOD2 negatively regulates antigen-presenting cell (APC) function during GVHD | 65 |