Adiponectin modulates inflammatory reactions via calreticulin receptor–dependent clearance of early apoptotic bodies
J. Clin. Invest. Yukihiro Takemura, et al. 117:375 doi:10.1172/JCI29709 [Go to this article.]

Figure 1
APN deficiency leads to the accumulation of apoptotic debris. (A) WT and APN-KO mice were treated with dexamethasone (DEX), and thymi were stained for apoptotic cells with TUNEL. In some experiments, mice received an i.v. infusion of Ad-APN or Ad–β-gal 2 days prior to injection of dexamethasone. The number of TUNEL-positive cells per microscopic field for the different experimental conditions is reported. *P < 0.05 versus WT; ^†P < 0.05 versus Ad–β-gal for WT or APN-KO (n = 3–6). (B) Adiponectin stimulates macrophage engulfment of TUNEL-positive apoptotic debris in thymi of dexamethasone-treated mice. Histological sections were stained with TUNEL (green) and anti-CD11b antibody (red). Scale bar: 20 μm. Colocalization is indicated by yellow in the merged images. ^††P < 0.01 versus Ad–β-gal for WT or APN-KO (n = 3–6). M, macrophage.