. Author manuscript; available in PMC: 2016 Jun 27.

Published in final edited form as: Nat Rev Nephrol. 2014 Sep 30;10(11):625–643. doi: 10.1038/nrneph.2014.170

Table 3.

Experimental models of murine glomerular disease with known DC- and Mac-related pathogeneses

Model	Mechanism	DC/Mac function
Nephrotoxic nephritis (NTN)⁸⁹	Glomerular injury- induced by the injection of mouse/rat renal cortex into a heterologous species (eg sheep, rabbits), then the Abs introduced into rodents	Ag/Ab complexes endocytosed by MHC II⁺ DC and Ag presented to CD4⁺ T cells. Mac are the main effector cells²⁰¹. Aggravation of damage after early depletion of CD11c⁺ DC⁹².
Glomerulonephritis – (NOH mice ¹⁰⁴)	Podocyte injury - the promoter for podocyte-specific human nephrin fused to cDNA encoding the transmembrane domain of the transferrin receptor, ovalbumin (OVA), and hen egg lysozyme (HEL)	Injection of activated OT-II (OVA-specific) Th cells, intra-renal stimulation. Periglomerular infiltrate, Mac-like: CD11c⁺, CD86⁺, MHC II⁺, CD11b^hi/int, Gr1⁺
Lupus models:
BWF1 mice ²⁰²	F1 hybrid strain created from mating New Zealand black and white mice²⁰⁵, ²⁰⁶	Mononuclear cell infiltration in kidney. Attraction of autoreactive T and B cells to kidney and expansion in draining lymph node¹¹⁴. CD11b⁺CD11c⁺ intrarenal DC/Mac are the source of B lymphocyte chemokine¹⁰⁶.
B6.TC mice²⁰³	Mice homozygous for the NZM2410 lupus susceptibility QTL (Sle1, Sle2 and Sle3)	DC from these mice demonstrate higher CD40 expression ²⁰⁷ DC have higher T cell allostimulatory capacity¹¹¹
NZM2328 mice ²⁰⁴	Derived by selective inbreeding of progeny of a cross between NZB and NZW mice	Intraglomerular CD11c⁺ DC, F4/80⁺ Mac are confined to interstitial regions