Table 2.

Kidney diseases and innate immunity

Disease or ConditionMolecules InvolvedCommentsReference
IgA nephropathyDefensin, TNFSF13Human, GWAS96
TLR9, MyD88Murine (ddYa), GWAS97
Diabetic nephropathyTLR4Human93
Kidney transplantTLR4, CD14, TLR3Human, polymorphisms61,102105
MyD88Murine106
Renal diseasebLPS-stimulated moleculesHuman98
GNTLR4, TLR2Murine (TSLP/FcƳRIIba, nephrotoxic serum)84,107,108
Hepatitis C–associated GNTLR3Human109
Lupus nephritisMyD88, TLR7, TLR9Murine (MRL/lpra)110112
NephrocalcinosisNLRP3Murine (calcium oxalate crystals)95
Cisplatin nephrotoxicityTLR4Murine59
Urinary obstructionTLR4Murine90
Polycystic kidney diseaseCD14Murine (cpka)113
Urinary tract infectionTLR4, TRIF, SIGIRRHuman114
TLR4, TLR5, TLR11Murine (E-coli)77,78,115118
ProteinuriaCD80, TLR4Murine (LPS)119
Sepsis-induced AKITLR4, TLR2, TLR9, MyD88Murine (LPS, CLP)57,120123
Ischemia-reperfusion injuryTLR4, TLR2, CD14, NLRP3, Nod1, Nod2Murine53,56,58,60,86,94,124–127
  • TNFS13, TNF ligand superfamily member 13; GWAS, genome-wide association study; MyD88, myeloid differentiation primary response gene 88; eQTL, expression quantitative trait loci; NLRP3, NOD-like receptor family, pyrin-domain-containing 3; SIGIRR, single immunoglobulin IL-1-related receptor; CLP, cecal ligation and puncture.

  • a Animal models for the indicated diseases.

  • b Enrichment of eQTL by GWAS ontology category “renal disease”.