Lymphoid neo-organogenesis: lymphotoxin's role in inflammation and development

Lymphoid organ development and inflammation have previously been considered as distinct mechanistically and functionally. In recent years, it has been realized that these phenomena have much in common. This insight has been gained from the recognition that cytokines of the lymphotoxin (LT)/tumor nec...

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Bibliographic Details
Published in:Immunologic research 1999-01, Vol.19 (2-3), p.119-125
Main Author: Ruddle, N H
Format: Article
Language:English
Subjects:
Animals
Autoimmunity
Embryonic and Fetal Development
Humans
Inflammation
Lymph Nodes - embryology
Lymph Nodes - immunology
Lymphotoxin-alpha - physiology
Mice
Rats
Tumor Necrosis Factor-alpha - physiology
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Summary:Lymphoid organ development and inflammation have previously been considered as distinct mechanistically and functionally. In recent years, it has been realized that these phenomena have much in common. This insight has been gained from the recognition that cytokines of the lymphotoxin (LT)/tumor necrosis factor (TNF) family are involved in both processes. The members of the family, LT-alpha, LT-beta, and TNF-alpha, and their multiple receptors participate combinatorially in lymphoid organ development and chronic inflammation. When inflammation that arises in microbial infection or autoimmune disease becomes chronic, it can take on the appearance of organized lymphoid tissue and has been called a tertiary lymphoid organ. Data with transgenic and knockout mice suggest that the process is cytokine-mediated and could be called "lymphoid neo-organogenesis." LT as LT-alpha3 and LT-alpha1beta2 plays a key role in these processes. Data obtained in vitro in an endothelial cell line and in vivo in transgenic and knockout mice indicate that LT influences these events through induction of adhesion molecules such as E-selectin adhesion molecule (ELAM), vascular cell adhesion molecule (VCAM), intercellular adhesion molecule (ICAM), mucosal addressin cellular adhesion molecule (MAdCAM), and peripheral node addressin (PNAd), and chemokines.
ISSN:0257-277X
DOI:10.1007/BF02786481