Open AccessAppearance and phenotype of murine follicular dendritic cells expressing VCAM‐1
Author(s) -
Balogh Péter,
Aydar Yüksel,
Tew John G.,
Szakal Andras K.
Publication year - 2002
Publication title -
the anatomical record
Language(s) - English
Resource type - Journals
eISSN - 1097-0185
pISSN - 0003-276X
DOI - 10.1002/ar.10148
Subject(s) - addressin , germinal center , follicular dendritic cells , vcam 1 , cell adhesion molecule , biology , stromal cell , population , antigen , high endothelial venules , spleen , dendritic cell , cell adhesion , immunology , b cell , microbiology and biotechnology , pathology , cell , t cell , icam 1 , antibody , antigen presenting cell , cancer research , immune system , medicine , genetics , environmental health
The architecture of lymphoid follicles is determined by a series of interactions between lymphoid and follicular stromal cells. A cardinal population in the non‐lymphoid compartment is the follicular dendritic cell (FDC), whose communication with resting and activated B cells involves various adhesive interactions. The FDC phenotype variably includes the display of vascular cell adhesion molecule (VCAM‐1). In this report we investigated the appearance and follicular tissue distribution of VCAM‐1 in murine peripheral lymphoid tissues, and compared VCAM‐1 with other FDC markers using immunohistochemistry. Correlating the appearance of VCAM‐1 with other murine FDC‐associated markers (CR1.2 [complement receptor 1.2 or CD35/21] and FDC‐M1) revealed that the display of VCAM‐1 is restricted to a subset of CR1.2‐positive FDCs. We found that the expression of VCAM‐1 antigen in the spleen or peripheral lymph nodes on FDCs requires antigenic stimulus, and that it coincides with germinal center formation. The VCAM‐1 expression is associated with the appearance of mucosal addressin cell adhesion molecule (MAdCAM‐1), with some slight differences in occurrence. The appearance of VCAM‐1 and MAdCAM‐1 antigens on FDCs may serve as indicators of FDC activation. Anat Rec 268:160–168, 2002. © 2002 Wiley‐Liss, Inc.