| pubmed-article:7782150 | pubmed:abstractText | The main purpose of this investigation was to determine whether exogenous triiodothyronine (T3) administered according to a protocol known to prevent depression in acquired immunity in weanling murine protein-energy malnutrition (PEM) would, likewise, influence the splenic natural killer (NK) cell in this disease. Weanling mice of disparate inbred strains, C57BL/6J and CBA/J, were subjected to wasting PEM produced by means of two low-protein diets (0.5% crude protein) identical in every respect except that one diet contained supplemental T3 (0.2 micrograms/g diet). NK cell lytic activity toward YAC-1 targets was assessed in vitro using suspensions containing 0.5 x 10(6) mononuclear spleen cells. Lytic activity in this assay was low in mice fed the unsupplemented low-protein diet, but was not depressed in malnourished animals given exogenous T3. Surface marker analysis using the NK cell-specific antigen, NK 1.1 (PK 136), revealed no effect of the low-protein diet or of exogenous T3 on the proportion of splenic mononuclear cells exhibiting NK 1.1+ phenotype. Previous investigations have shown that acquired immune competence in PEM can be manipulated, by means of endocrine hormonal intervention, independently of continued wasting disease. The present results extend this fundamental new concept to include an innate immune function, namely NK cell lytic activity. In this system of experimental PEM, exogenous T3 prevented depression in NK cell lytic activity expressed on a per cell basis. The malnourished weanling rodent is a particularly powerful experimental system with which to investigate the mechanisms whereby thyroid hormones influence NK cells. | lld:pubmed |
