Table A1.
Involvement of KLF2 in selected diseases.
| Disease | Involvement of KLF2 | KLF2-Related Effects | Cell Type | Refs. |
|---|---|---|---|---|
| HIV-1 infection | KLF2 downregulation -> S1PR1 and L-Selectin downregulation/CD69 upregulation | Defective CD4+ T cell migration | CD4+ T cells | [76,77] |
| Autoimmunity | KLF2 knockout (Foxp3-cre deleter) | Signs of psoriasis, signs of IBD | iTregs | [69] |
| Type1 Diabetes (Autoimmunity) | microRNA-92a regulating KLF2 -> dysregulated TFH precursor pool size | Autoimmunity against insulin producing beta-cells | TFH | [78] |
| Allergic Asthma | Notch knockout (CD4-cre deleter) -> downregulation of KLF2 -> downregulation of S1PR1 | Th2 cells are primed to leave the lymph node and invade the lung by KLF2-mediated upregulation of S1PR1; KLF2 downregulation by Notch-deficiency prevents Th2 lung infiltration | Th2 cells | [79] |
| Asthma | reduced KLF2 expression in blood neutrophils of Asthma patients -> upregulation of CXCR1 and CXCR2 | Enhanced neutrophil migration | Neutrophils | [97] |
| Arthritis | Hemizygous KLF2 mice | Increased pro-inflammatory factors, osteoclast differentiation | Monocytes, Osteoclasts | [88] |
| Marginal Zone B cell Lymphoma | KLF2 knockout (mb1-cre deleter, CD19-cre deleter) & KLF2 mutations in human SMZBL -> strongly enriched MZB pool size | Splenomegaly (mouse),Marginal Zone B cell Lymphoma (human) | B cells | [8,10,18,19,21] |
| Atherosclerosis | KLF2 knockout (LysM-cre deleter) on Ldlr-deficient background; hemizygous KLF2 on ApoE-deficient background | Increased adhesion to endothelial cells, Increased signs of atherosclerosis when combined with Ldlr-deficiency or ApoE-deficiency | Macrophages/Neutrophils | [93,94] |
| Atherosclerosis | KLF2 knockout (CD11c-cre deleter) -> CD86 and CD40 upregulation upon LPS activation | Enhanced T cell activation, Increased signs of atherosclerosis when combined with Ldlr-deficiency | Dendritic cells | [98] |
| Thrombosis | KLF2 knockout (LysM-cre deleter) -> decreased P-Selectin | Decreased rolling ability | Neutrophils | [96] |
| Muscle Injury | KLF2 knockout (LysM-cre deleter) -> CCR5 upregulation | Increased numbers of CCR5+ monocytes and of MerTK+ macrophages in injured muscles -> increased phagocytosis activity | Macrophages | [95] |
| Sepsis | KLF2 knockout (Lyz2-cre deleter) | Endotoxic shock | Myeloid cells | [90] |