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B2–/– Mice Causes Impaired Lymph Node Development and Lymphocyte Recruitment1
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* Department of Anatomy,
Division of Infection and Immunity,
Medical Research Council Centre for Immune Regulation, and
Cancer Research United Kingdom Institute for Cancer Studies, The Medical School, University of Birmingham, Edgbaston, Birmingham, United Kingdom
The NF-
B family of transcription factors is vital to all aspects of immune function and regulation in both the hemopoietic and stromal compartments of immune environments. Recent studies of mouse models deficient for specific members of the NF-B family have revealed critical roles for these proteins in the process of secondary lymphoid tissue organogenesis. In this study, we investigate the role of NF-B family member NF-B2 in lymph node development and lymphocyte recruitment. Inguinal lymph nodes in nfb2–/– mice are reduced in size and cellularity, most notably in the B cell compartment. Using in vitro and in vivo lymph node grafting assays, we show that the defect resides in the stromal compartment. Further examination of the nfb2–/– inguinal lymph nodes revealed that expression of peripheral node addressin components CD34 and glycosylation-dependent cell adhesion molecule-1 along with the high endothelial venule-restricted sulfotransferase HEC-GlcNAc6ST was markedly reduced. Furthermore, expression of the lymphocyte homing chemokines CCL19, CCL21, and CXCL13 was down-regulated. These data highlight the role of NF-B2 in inguinal lymph node organogenesis and recruitment of lymphocytes to these organs due to its role in up-regulation of essential cell adhesion molecules and chemokines, while suggesting a potential role for NF-B2 in organization of lymph node endothelium.
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