Increased DC trafficking to lymph nodes and contact hypersensitivity in junctional adhesion molecule-A–deficient mice
J. Clin. Invest. Maria Rosaria Cera, et al. 114:729 doi:10.1172/JCI21231 [Go to this article.]

Figure 2
Histological analysis of Jam-A ^–/– and endothelial Jam-A ^–/– mice. (A) Immunofluorescence staining of serial cryosections of Jam-A^+/+, Jam-A ^–/–, and endothelial Jam-A ^–/– (Tie-2 Cre Jam-A ^–/–) kidneys using anti-PECAM and anti–JAM-A (BV12) Ab’s. All sections show positive staining for PECAM (both controls and mutants), while JAM-A staining is undetectable in all type of tissues in Jam-A ^–/– mice. Note that endothelial cells from Tie-2 Cre Jam-A ^–/– animals are negative for JAM-A staining (arrow). The arrowheads indicate that JAM-A staining on the epithelium of the tubuli is still detectable. Staining is weaker compared with Jam-A^+/+ mice since the peritubular capillaries are negative. Scale bar: 200 μm. (B) Immunostaining of serial cryosections of aorta from Jam-A^+/+ and Tie-2 Cre Jam-A ^–/– mice, using anti-PECAM and anti–JAM-A (BV12) Ab’s. Vascular endothelial JAM-A is undetectable in Tie-2 Cre Jam-A ^–/– aorta. Scale bar: 200 μm. (C) Cryosections of Jam-A^+/+ and Tie-2 Cre Jam-A ^–/– lymph nodes were double stained for LYVE (in green), a marker of lymphatic endothelial cells, and for JAM-A (in red). In Jam-A^+/+ mice, the colocalization of JAM-A and LYVE is evident; this was not observed in Tie-2 Cre Jam-A ^–/– animals. Scale bar: 50 μm.