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 [
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Figure 9Morphology, JAM-A expression, and DC distribution in lymph node and skin sections. (
A) H&E staining of a lymph node section from a
Jam-A –/– mouse displays normal architecture including cortical lymphoid nodules (CN) and an expanded paracortical area (PC); PC is populated by DCs, highlighted by their strong expression of MHC class II molecule (inset). (
B) Expression of JAM-A in a lymph node section from a
Jam-A+/+ mouse is evident in sinus macrophages (asterisk), high endothelial venules (arrowheads in
B and
C), and DCs in the paracortex (
C, black arrow). (
D) In normal skin, a diffuse JAM-A expression is observed in epidermal and pilar keratinocytes, in endothelial cells of dermal vessels (arrowhead), and in scattered fusate/stellate dermal cells (inset). (
E) A skin section from a
Jam-A –/– mouse illustrates the regular distribution of MHC class II
+ LCs; LCs display an evident dendritic morphology with fine and long dendrites, and express Langerin (insert). (
F and
G) Sections from an inguinal lymph node obtained after FITC skin painting display green-dotted FITC
+ cells in the paracortex that coexpress JAM-A (
F, arrow) and Langerin (
G, arrow). MHC class II
+ and JAM-A
+ cells were detected by immunoperoxidase technique as seen in
A (inset),
B,
C, and
D. Immunofluorescence staining was used to detect JAM-A
+ cells (red cells in
F), MHC class II
+ LCs (red cells in
E), and Langerin
+ LCs (red cells, inset in
E;
G). Magnification: ×40 in
A, ×200 in
F and
G, ×400 in
B,
D, and
E, and ×600 in insert in
A,
C, insert in
D, and insert in
E. Scale bars: 500 μm in
A, 50 μm in
B, 20 μm in
C, and 100 μm in
F.
