Table 1.
Animal models with ischemia/reperfusion (I/R) injury in separate organs, either the heart or kidney
| First author [Ref.], year | Models | Species | Major findings | Pathogenic implications |
|---|---|---|---|---|
| Zhang [21], 1993 | Myocardial ischemic injury | Male SD rats | Significant increase in OX6+ DCs (MHC II), ED2+ macrophages, and W3/25+ T help cells; peaked at days 7–14 | Cardiac ischemia activates DCs and resultant immune response |
| Naito [22], 2008 | Myocardial ischemic injury | Male Wistar rats | The increased numbers of OX62+ DCs, heat shock protein 70, TLR2 and TLR4, and IFN-γ expression are reduced by G-CSF; IL-10 expression is increased by G-CSF and decreased by GM-CSF | Cardiac DCs exert modulating effects on LV remodeling MI by G-CSF improvement or GM-CSF exacerbation |
| Kim [55], 2005 | Renal I/R injury | Male SD rats | Significant increase in OX6+ DCs (MHC II) and OX62+ DCs, peaking at days 3–5 after I/R injury; renal I/R injury increases TLR2 and TLR4 mRNA protein expression; renal I/R also reduces TLR ligand (HSP70) | Renal I/R injury rapidly activates innate immune response |
| Wu [56], 2006 | Renal I/R injury | SD rats | Significant increase in peripheral blood monocyte-derived DCs, expression of DC surface markers of CD11c, CD80, CD86, MHC II (LA), and IL-12 production at day 2 after I/R injury | DC progenitors migrate to kidney via peripheral blood following I/R injury |
| Wu [57], 2006 | Renal I/R injury | SD rats | Significant decrease in bone marrow-derived DCs, but increase in peripheral blood monocyte-derived DCs; increase in CD11c+, CD80+, and CD86+ DCs in the outer medulla of the injured kidney | Bone marrow DC progenitors migrate to the outer medulla (the area susceptible to I/R injury) of the kidney following I/R injury |
| Di Giorno [58], 2006 | Renal I/R injury | Male C57BL 6 mice | Renal I/R injury increases CD11c+ DCs, CD4+ and CD8+ T cells, and upregulates expression of MHC class I and II molecules; N-acetyl-cysteine reduces CD11c+ DCs and MHC class II expression | N-acetyl-cysteine decreases renal DC infiltration |
| Dong [60], 2007 | Renal I/R injury | C57BL/mice | Renal F4/80+ DCs are predominant TNF-α-secreting cells in early renal I/R injury | Renal DCs contribute to early release of innate immune response to I/R injury |
| Kim [59], 2010 | Renal I/R injury | C57BL/6 mice | CD11c+ F4/80+ DC depletion induces higher tissue levels of pro-inflammatory cytokines and lower level of IL-10 | Renal CD11c+/F4/80+ DC subset contribute to the recovery process of AKI |
DCs, dendritic cells; G-CSF, granulocyte colony-stimulating factor; GM-CSF, granulocyte-macrophage colony-stimulating factor; SD, Sprague-Dawley; LV, left ventricle; MHC, major histocompatibility complex; TLR2 or TLR4, Toll-like receptor 2 or 4.