Tumor necrosis factor alpha is involved in mouse growth and lymphoid tissue development
Details
Serval ID
serval:BIB_BE38F7A75D99
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Tumor necrosis factor alpha is involved in mouse growth and lymphoid tissue development
Journal
Journal of Experimental Medicine
ISSN
0022-1007 (Print)
Publication state
Published
Issued date
11/1992
Volume
176
Number
5
Pages
1259-64
Notes
Journal Article
Research Support, Non-U.S. Gov't --- Old month value: Nov 1
Research Support, Non-U.S. Gov't --- Old month value: Nov 1
Abstract
Tumor necrosis factor alpha (TNF-alpha), a major mediator of inflammation, also possesses a wide pleiotropism of actions, suggesting its involvement in physiological conditions. TNF-alpha mRNA is present in mouse embryonic tissues and also in fetal thymus and spleen. Repeated injections of a monospecific polyclonal rabbit anti-mouse TNF-alpha antibody in mice, starting either during pregnancy or at birth, led to a severe but transient growth retardation, already present at birth, reaching a 35% decrease in body weight at 3 wk, with complete recovery at 8 wk. The insulin growth factor I (IGF-I) blood levels were decreased to about 50%; growth hormone release and other endocrine functions were unaltered. A marked atrophy of the thymus, spleen, and lymph nodes was also observed, with lymphopenia and impaired development of T and B cell peripheral lymphoid structures. The pathways involving TNF-alpha in IGF-I release and early body growth are probably distinct from those by which TNF-alpha participates in early development of lymphoid tissues, where its low physiological release may contribute to enhance lymphoid cell expansion.
Keywords
Animals
Antibodies/immunology
Female
*Growth
Growth Hormone/blood
Insulin-Like Growth Factor I/analysis
Lymphocytes/physiology
Lymphoid Tissue/*physiology
Mice
Pregnancy
Tumor Necrosis Factor-alpha/genetics/*physiology
Pubmed
Web of science
Open Access
Yes
Create date
15/02/2008 17:57
Last modification date
20/08/2019 16:32