Table 1.
The effects of damage-associated molecular patterns in HBV-related liver injury.
| DAMPs | Effects in HBV-related liver injury | References |
|---|---|---|
| HSP | To support the process of HBV replication Induction of nonspecific immunity Upregulation of antigen-specific cytotoxic T lymphocyte response |
[21–32] |
|
| ||
| UA | To trigger innate immunity To act as adjuvants to enhance the HBsAg-specific-CTL cytotoxicity |
[34, 38] |
|
| ||
| NA | Stimulation of TLR-associated signaling pathways To induce an array of proinflammatory cytokines |
[39–43] |
|
| ||
| HMGB1 | To elicit innate and adaptive immune response To impair the immune regulatory effect of Treg cells Collaboration with other DAMPs to potentiate inflammation |
[48, 50–52] [17, 54, 62–66] |
|
| ||
| IL-33 | Upregulation of Th2-polarized response To protect the survival of hepatocytes Suppress the secretion of HBsAg and HBeAg and HBV DNA replication in vitro |
[73, 74, 76] |
CTL: cytotoxic T lymphocyte; DAMP: damage-associated molecular pattern; DNA: deoxyribonucleic acid; HBeAg: hepatitis B e-antigen; HBsAg: hepatitis B surface antigen; HBV: hepatitis B virus; HMGB-1: high mobility group box 1; HSP: heat shock protein; NA: nucleic acid; Treg: T regulatory; UA, uric acid.