title: Influence of thyroxine and thyroxine with growth hormone and prolactin on splenocyte subsets and on the expression of interleukin-2 and prolactin receptors on splenocyte subsets of Snell dwarf mice.
abstract: A number of immune parameters were examined in Snell dwarf mice and compared with normal littermates. The number of splenocytes per gram of body weight were significantly decreased in dwarf animals, and the decrease was distributed throughout the CD4, CD8, B220, and MAC-1 subsets. The percentage of CD4 and CD8 splenocytes was markedly increased, and the percentage of B220 and MAC-1 splenocytes markedly decreased, in dwarf animals. In addition, the percentage of splenocyte T cells constitutively expressing interleukin-2 (IL-2) receptors and prolactin (PRL) receptors was decreased, with the CD4 subset presenting the most dramatic effect. The effects of replacing the hormones deficient in the Snell dwarf mouse (i.e., growth hormone [GH], prolactin [PRL], and thyroxine [T4] on the above immune parameters were also examined. The administration of T4 alone for 10 days corrected the defect in splenocyte cell numbers per grams body weight for both the CD4 and CD8 subsets, but only partially corrected the defect for the B220 and MAC-1 subsets. The addition of rbGH and rbPRL for the last 3 days of T4 injection had little additive effect on the number of CD4 and CD8 cells but increased the number of B220 and MAC-1 subsets to values comparable to those of normal animals on the basis of body weight. The decrease in the percentage of CD4 splenocytes in dwarf animals constitutively expressing IL-2R was partially corrected by T4 injection and completely corrected by the addition of rbGH and rbPRL for the last 3 days. The decrease in CD4 splenocytes constitutively expressing PRLR was partially corrected by T4 injection alone and the addition of rbGH and rPRL resulted in percentages comparable to that of normal animals. The results indicate that Snell dwarf animals are deficient in immune parameters and that the administration of the hormones lacking in this animal can correct the deficiencies.
authors.affiliation: Department of Physiology, Wayne State University, School of Medicine, Detroit, Michigan 48201, USA.
authors.forename: R R
authors.initials: RR
authors.lastname: Gala
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D001835:Body Weight / Q000187:drug effects; D004347:Drug Interactions; D004392:Dwarfism; D005434:Flow Cytometry; D013006:Growth Hormone / Q000494:pharmacology*; D007376:Interleukin-2 / Q000096:biosynthesis*; D051379:Mice; D008809:Mice, Inbred C3H; D008817:Mice, Mutant Strains; D011388:Prolactin / Q000494:pharmacology*; D011981:Receptors, Prolactin / Q000096:biosynthesis*; D012016:Reference Values; D013154:Spleen / Q000276:immunology; D016176:T-Lymphocyte Subsets / Q000187:drug effects / Q000276:immunology* / Q000378:metabolism*; D013974:Thyroxine / Q000494:pharmacology*; D015430:Weight Gain
chemical_list: D007376:Interleukin-2; D011981:Receptors, Prolactin; D011388:Prolactin; D013006:Growth Hormone; D013974:Thyroxine