Influence of dietary protein restriction on immune competence. II. Effect on lymphoid tissue
Weanling mice fed a 4 percent diet showed a generalized loss of lymphoid tissue which was greater than the loss of total body weight. This effect was greatest in the thymus greater than spleen greater than mesenteric lymph node. Cell loss was most pronounced during the 1st week on diets, then remain...
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Published in | Clinical and experimental immunology Vol. 26; no. 2; pp. 314 - 326 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
England
01.11.1976
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Subjects | |
Online Access | Get full text |
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Summary: | Weanling mice fed a 4 percent diet showed a generalized loss of lymphoid tissue which was greater than the loss of total body weight. This effect was greatest in the thymus greater than spleen greater than mesenteric lymph node. Cell loss was most pronounced during the 1st week on diets, then remained at stable levels for 3 weeks and showed a gradual rise thereafter. The effect was shown to be mediated partly by a cessation of growth in lymphoid organs due to the low protein intake and, secondly, an adrenal corticosteroid induced lympholysis which actually reduced cell numbers. Recirculating T cells and resident B cells were amongst the least affected cells whereas stem cells, non-migratory T cells and other reticuloendothelial cells were most depressed in numbers. At no stage was the germinal centre forming capacity of the mesenteric node lost although cell recruitment to antigenically stimulated nodes was diminished. During nutritional repletion the spleen, thymus and mesenteric node all showed different and characteristic regrowth. The spleen was most active initially and rapidly reconstituted haemopoietic cells and B cells. This was followed by the thymus which showed a delayed reinitiation of its normal growth kinetics which had been interrupted by the diet. The evidence suggested that full rehabilitation of the immune apparatus took place even after 2 months of nutritional deprivation. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0009-9104 1365-2249 |