Histochemical studies of high-endothelial venules of lymph nodes and peyer's patches in the mouse

1972 ◽  
Vol 131 (3) ◽  
pp. 287-297 ◽  
Author(s):  
C. R�pke ◽  
O. J�rgensen ◽  
M. H. Cla�sson
Keyword(s):  
Lymph Nodes ◽  
Peyer's Patches ◽  
Peyer’S Patches ◽  
High Endothelial Venules

CD4+ T cells of both the naive and the memory phenotype enter rat lymph nodes and Peyer's patches via high endothelial venules: Within the tissue their migratory behavior differs

1997 ◽  
Vol 27 (12) ◽  
pp. 3174-3181 ◽  
Author(s):  
Jürgen Westermann ◽  
Ulrike Geismar ◽  
Angélique Sponholz ◽  
Ulrike Bode ◽  
Sheila M. Sparshott ◽  
...  
Keyword(s):  
T Cells ◽  
Lymph Nodes ◽  
Cd4 T Cells ◽  
Peyer's Patches ◽  
Migratory Behavior ◽  
Peyer’S Patches ◽  
High Endothelial Venules ◽  
Memory Phenotype

scholarly journals Chemokine Requirements for B Cell Entry to Lymph Nodes and Peyer's Patches

2002 ◽  
Vol 196 (1) ◽  
pp. 65-75 ◽  
Author(s):  
Takaharu Okada ◽  
Vu N. Ngo ◽  
Eric H. Ekland ◽  
Reinhold Förster ◽  
Martin Lipp ◽  
...  
Keyword(s):  
Lymph Nodes ◽  
B Cell ◽  
Chemokine Receptor ◽  
Cell Entry ◽  
Peyer's Patches ◽  
Peyer’S Patches ◽  
Wild Type ◽  
High Endothelial Venules ◽  
Cell Homing ◽  
T Cell Homing

B cell entry to lymph nodes and Peyer's patches depends on chemokine receptor signaling, but the principal chemokine involved has not been defined. Here we show that the homing of CXCR4−/− B cells is suppressed in CCL19 (ELC)- and CCL21 (SLC)-deficient paucity of lymph node T cells mice, but not in wild-type mice. We also find that CXCR4 can contribute to T cell homing. Using intravital microscopy, we find that B cell adhesion to high endothelial venules (HEVs) is disrupted when CCR7 and CXCR4 are predesensitized. In Peyer's patches, B cell entry is dependent on CXCR5 in addition to CCR7/CXCR4. CXCL12 (SDF1) is displayed broadly on HEVs, whereas CXCL13 (BLC) is found selectively on Peyer's patch follicular HEVs. These findings establish the principal chemokine and chemokine receptor requirements for B cell entry to lymph nodes and Peyer's patches.

Virus-associated activation of innate immunity induces rapid disruption of Peyer’s patches in mice

Blood ◽  
2013 ◽  
Vol 122 (15) ◽  
pp. 2591-2599 ◽  
Author(s):  
Simon Heidegger ◽  
David Anz ◽  
Nicolas Stephan ◽  
Bernadette Bohn ◽  
Tina Herbst ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Virus Infection ◽  
Lymph Nodes ◽  
Immune Activation ◽  
Innate Immune ◽  
Peyer's Patches ◽  
Peyer’S Patches ◽  
Type I ◽  
Peripheral Lymph ◽  
Key Points

Key Points Systemic virus infection leads to rapid disruption of the Peyer’s patches but not of peripheral lymph nodes. Virus-associated innate immune activation and type I IFN release blocks trafficking of B cells to Peyer’s patches.

scholarly journals Rapid G protein-regulated activation event involved in lymphocyte binding to high endothelial venules.

1993 ◽  
Vol 178 (1) ◽  
pp. 367-372 ◽  
Author(s):  
R F Bargatze ◽  
E C Butcher
Keyword(s):  
G Protein ◽  
Pertussis Toxin ◽  
Critical Role ◽  
Lymphocyte Activation ◽  
Inhibitory Effect ◽  
Peyer's Patches ◽  
Peyer’S Patches ◽  
High Endothelial Venules ◽  
Activation Event

The homing of blood borne lymphocytes into lymph nodes and Peyer's patches is mediated in part by recognition and binding to specialized high endothelial venules (HEV). Here we demonstrate that a rapid pertussis toxin-sensitive lymphocyte activation event can participate in lymphocyte recognition of HEV. In situ video microscopic analyses of lymphocyte interactions with HEV in exteriorized mouse Peyer's patches reveal that pertussis toxin has no effect on an initial "rolling" displayed by many lymphocytes, but inhibits an activation-dependent "sticking" event required for lymphocyte arrest. This is the first demonstration that physiologic lymphocyte-endothelial interactions can involve sequential rolling, activation, and activation-dependent arrest, previously shown only for neutrophils. The inhibitory effect of the toxin is dependent on its G protein-modifying ADP-ribosyltransferase activity and can be reversed by phorbol myristic acetate, which bypasses cell surface receptors to trigger activation-dependent adhesion. Lymphocyte sticking can occur within 1-3 s after initiation of rolling. We conclude that a rapid receptor-mediated activation event involving G protein signaling can trigger stable lymphocyte attachment to HEV in vivo, and may play a critical role in regulating lymphocyte homing.

Sign in / Sign up

Export Citation Format

Share Document