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- [1] IL-12 deficiency in MRL-Faslpr mice delays nephritis and intrarenal IFN-γ expression, and diminishes systemic pathology JOURNAL OF IMMUNOLOGY, 2003, 170 (07): : 3915 - 3925
- [2] IL-34-Dependent Intrarenal and Systemic Mechanisms Promote Lupus Nephritis in MRL-Faslpr Mice JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY, 2019, 30 (02): : 244 - 259
- [4] IL-12 drives IFN-γ-dependent autoimmune kidney disease in MRL-Faslpr mice JOURNAL OF IMMUNOLOGY, 1999, 163 (12): : 6884 - 6891
- [5] Intra-renal IL-18 triggers systemic lupus, while caspase-1 inhibition ameliorates IL-18 mediated nephritis in MRL-Faslpr mice ZEITSCHRIFT FUR RHEUMATOLOGIE, 2013, 72 : 142 - 142
- [7] Intra-renal IL-18 Triggers Systemic Lupus, while Caspase-1 Inhibition Ameliorates IL-18 Mediated Nephritis in MRL-Faslpr mice. INTERNIST, 2013, 54 : 8 - 8
- [8] Intra-renal IL-18 Triggers Systemic Lupus, while Caspase-1 Inhibition Ameliorates IL-18 Mediated Nephritis in MRL-Faslpr mice. INTERNIST, 2013, 54 (06): : 744 - 744
- [9] γδT Cells Positively Regulate Contact Sensitivity (CS) Reaction via Modulation of INF-γ, IL-12 and TNF-α Production FOLIA BIOLOGICA-KRAKOW, 2013, 61 (3-4): : 205 - 210