title: Humoral immune response in mice over-expressing or deficient in growth hormone.
abstract: Effects of growth hormone (GH) levels on the humoral immune response were investigated in metallothionein I (MT)-bovine (b) GH-transgenic (tg) and GH-deficient Ames dwarf (Prop1 df(-/-)) mice. Four-month-old mice were given primary and secondary injections of either normal saline or tetanus toxoid (TT) to induce specific antibody (Ab) production. MT-bGH-tg mice with high peripheral levels of bGH produced less TT-specific Ab than normal nontransgenic (Ntg) littermates, df, or nondwarf (Ndf) control mice. Titers reached maximum levels at 3-4 weeks post-primary immunization (PPI) and declined gradually through 24 weeks PPI in all groups of mice. Peripheral CD4(+) and CD8(+) T cell populations were significantly lower in tg than in Ntg, df, or Ndf mice. No significant differences were found in B cell numbers between tg, Ntg, or df mice. T helper 2 (Th2) cell populations were significantly greater in df mice compared to Ntg control mice. No significant differences were found in CD4(+):CD8(+) T cell ratios, interleukin (IL)-4 concentrations or interferon (IFN)-gamma levels between tg,Ntg, df, and Ndf mice. No patterns of significant sexual dimorphism were found for any of the immune parameters studied. Elevated levels of corticosterone were investigated as a possible immunosuppressant mechanism responsible for low Ab responses in the tg mice. Ab production was not enhanced by decreasing corticosterone in tg mice. Thus, high endogenous GH levels inhibit specific Ab production and peripheral T cell populations but not peripheral B cell numbers, Th2 cell populations, or IL-4 or IFN-gamma production. Elevated corticosterone levels do not appear to be responsible for suppressed humoral immune responses. Low levels of endogenous GH do not inhibit specific Ab production but may contribute to increased peripheral Th2 cell numbers.
authors.affiliation: Research Services, Department of Veterans Affairs Medical Center, Memphis, TN 38104, USA.
authors.forename: Mary A
authors.initials: MA
authors.lastname: Hall
authors.forename: Andrzej
authors.initials: A
authors.lastname: Bartke
authors.forename: John M
authors.initials: JM
authors.lastname: Martinko
mesh_terms: D000315:Adrenalectomy; D000818:Animals; D000917:Antibody Formation / Q000502:physiology*; D003345:Corticosterone / Q000378:metabolism; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D013006:Growth Hormone / Q000172:deficiency / Q000502:physiology*; D007108:Immune Tolerance / Q000502:physiology; D007074:Immunoglobulin G / Q000096:biosynthesis; D007371:Interferon-gamma / Q000378:metabolism; D015847:Interleukin-4 / Q000378:metabolism; D008214:Lymphocytes / Q000276:immunology* / Q000378:metabolism; D008297:Male; D051379:Mice; D008809:Mice, Inbred C3H; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D008822:Mice, Transgenic; D013745:Tetanus Toxoid / Q000378:metabolism / Q000494:pharmacology; D018417:Th1 Cells / Q000378:metabolism; D018418:Th2 Cells / Q000378:metabolism
chemical_list: D007074:Immunoglobulin G; D013745:Tetanus Toxoid; D015847:Interleukin-4; D007371:Interferon-gamma; D013006:Growth Hormone; D003345:Corticosterone