Table 4.
The phenotypes of chemokine ligands and receptors gene-modified mice in RA models.
| Gene | RA model and phenotypes |
|---|---|
| CCL3 | CCL3 KO mice (C57BL/6 background) showed a mild arthritis and decreased serum amyloid P level in CAIA |
| CCL19, CCL21 | plt/plt mice, a naturally occuring CCL19 and CCL21 mutation strain (B6N.DDD-plt/NknoJ), showed a mild arthritis in CIA |
| CXCL10 | CXCL10 KO mice (C57BL/6 mice) showed mild arthritis, and decrease of macrophage and T cell accumulation in arthritic joints in CAIA |
| CXCL14 | CXCL14 Tg mice (C57BL/6 background) showed severe arthritis and increased T cell and B cell response in CIA |
| CCR2 | CCR2 KO mice (C57BL/6 background) showed decrease of neutrophil recruitment into the joints in AIA |
| CCR2 KO mice (DBA/1J background) showed severe arthritis in CIA and increase of Th17 cell population, autoantibody production, and neutrohpil infiltration into joints in CIA | |
| CCR2 KO mice (DBA/1J, but not BALB/c background) developed arthritis than WT mice in CIA with cutaneous M. avium infection | |
| CCR2 KO mice (DBA/1J background) showed severe arthritis and elevated autoantibody production in CIA | |
| CCR2 KO mice (DBA/1J background) showed severe arthritis in CAIA and enhanced protease activation from monocytes and neutrophils in CAIA | |
| CCR2 deficiency promoted spontaneous arthritis development and neitrophil infiltration into joints in IL-1R antagonist KO mice (BALB/c background) | |
| CCR4 | CCR4 KO mice (C57BL/6 background) showed mild arthritis via inhibition of Th17 cell expansion in CIA |
| CCR5 | CCR5 KO mice (DBA/1J background) showed mild arthritis and decrease of autoantibody production in CIA |
| CCR5 KO mice (DBA/1J background) showed comparable severity with WT mice in CIA | |
| CCR6 | CCR6 KO mice (C57BL/6 background) showed mild arthritis and decrease of autoantibody production in CIA |
| CCR6 KO mice (C57BL/6 background) showed comparable severity with WT mice in K/BxN | |
| CCR6 deficiency did not affect the arthritis development in spontaneous RA model, human TNF-α Tg mice (C57BL/6 background) | |
| CCR7 | CCR7 KO mice (C57BL/6 background) showed a completely resistance to arthritis and decrease of autoantibody production in CIA, via inhibition of DC chemotactic ability |
| CCR7 KO mice (C57BL/6 background) showed mild arthritis, decrease of autoantibody production and T cell proliferation in AIA | |
| CCR9 | CCR9 KO mice (C57BL/6 background) showed mild arthritis and inhibition od CD11c-positive splenocyte migration in CIA |
| CXCR3 | CXCR3 KO mice (C57BL/6 mice) showed mild arthritis, and decrease of macrophage and T cell accumulation in arthritic joints in CAIA |
| CXCR4 | CXCR4 KO mice (DBA/1 background) showed resistance to arthritis in CIA |
| CXCR5 | CXCR5 KO mice (C57BL/6 background) showed mild arthritis, decrease of autoantibody production and T cell proliferation in AIA |
| CXCR5 null KO mice (C57BL/6 background) showed completely resistance to arthritis and decrease of autoantibody production, but did not affect leukocyto migration into joints in CIA | |
| B cell-specific CXCR5 KO mice (C57BL/6 background) showed mild arthritis and decrease GC formation in CIA | |
| T cell-specific CXCR5 KO mice (C57BL/6 background) showed completely resistance to arthritis and decrease GC formation in CIA | |
| CXCR6 | CXCR6 KO mice (C57BL/6 background) showed resistance to arthritis and decrease leukocyto recruitment in K/BxN |
| CXCR6 KO mice (C57BL/6 background) showed resistance to arthritis and impaired cytokine polarization in T cells in CIA |