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Results for “Immune function”

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At least 1,333 records · Page 74Linked to original sources
PubMed1979

The role of corticosterone in the loss in immune function in the zinc-deficient A/J mouse.

Previous studies from this laboratory have shown that zinc deficiency causes rapid atrophy of the thymus with subsequent loss of T-cell helper function in the young adult A/J mouse. The purpose of this investigation was to determine if zinc deficiency constituted a chronic stress on the mouse leading to the elevation of glucocorticoid levels which is known to destroy thymic lymphocytes. The results of these experiments indicate that zinc-deficient mice indeed have increased levels of plasma corticosterone (115 mug/100 ml plasma) compared to mice fed zinc-adequate diets (40 mug/100 ml plasma). A significant reduction in T-cell helper function, which occurred 4 days after this rise in steroid concentration, suggests that corticosterone may contribute to the loss in immunity; however, about half of the total loss in T-cell helper function occurred prior to the increase in plasma corticosterone and was due to other factors associated with the lowered zinc levels.

Animals↗
PubMed1997

Immune function of prolactin (PRL) and signal transduction by PRL/GH/cytokine receptors: specificity, redundancy and lessons from chimaeras.

Although prolactin (PRL) was originally regarded exclusively as a lactogenic hormone, there are a number of observations that suggest a role for this protein in the regulation of immune responses. The first step in understanding this unexpected function came from the cloning of the prolactin receptor, which was later shown to be a member of the cytokine receptor superfamily. The PRL receptor shares structural analogies with receptors for proteins acting on immune cells, the prototype of which is IL-2. Studies of cytokine receptor signalling revealed that all messages are transmitted in the cell through a limited set of transducers, among which the JAK kinases and the Stat transcription factors represent a major cascade. Deciphering the rules allowing a given cytokine receptor, and not another, to activate a particular set of JAK and Stat proteins is a key step in understanding functional specificities within this receptor superfamily. Mutational analyses have provided interesting information about which features are required for which property. Much less data are available from studies using chimaeric receptors, although this strategy is probably more powerful for comparing different receptors and addressing the question of their specificity (or redundancy). As frequently as possible, we shall illustrate our discussions through experimental investigations using the chimaeric approach.

Animals↗
PubMed2005

Effects of dietary conjugated linoleic acid supplementation on performance and immune function of weaned pigs.

Two experiments were conducted to evaluate the effect of dietary conjugated linoleic acid (CLA) on performance and immune responses of weaned pigs. In Exp. I, 72 crossbred pigs weaned at 19 to 23 days of age and weighing 7.20 +/- 0.11 kg were randomly allotted to four diets supplemented with CLA at 0, 1, 2 or 3%. On day 14, pigs were injected with ovalbumin (1mg per kg BW) and blood samples were collected on day 7 and 14 after injection to test the specific OVA antibody. In Exp. II, 36 crossbred pigs weaned at 26 to 30 days of age and weighing 8.12 +/- 0.14 kg were randomly divided into two diets containing either 0 or 2% CLA. On day 14 and 28, blood samples were obtained to determine the lymphocyte proliferation and PGE2 levels in both trials, and CD4+, CD8+ T cells subsets and interleukin-1beta production were tested in Exp. II. In Exp. I both average daily gain and average daily feed intake of weaned pigs were improved quadratically and feed efficiency was increased linearly by CLA supplementation. Lymphocyte proliferation response to concanavalin A was increased quadratically as dietary CLA concentration increased on day 14 and 28. Ovalbumin antibody production levels were increased linearly on day 7 after injection of ovalbumin and increased quadratically on day 14 after injection, which follows the increased CLA levels, whereas CLA reduced linearly the production of prostaglandin E2 (PGE2). The results of Exp. II indicated that CLA improved performance, lymphocyte proliferation, and increased the CD8+ lymphocyte population, while reduced the production of PGE2 and interleukin-lbeta (IL- 1beta). These results suggest that the supplementation of CLA enhanced lymphocyte proliferation function, possibly by regulating the PGE2 production, and improved growth performance of pigs. Further studies are needed to determine the mechanism of CLA-induced inhibition of IL-1beta production.

Animal Feed↗
PubMed1985

Neural modulation of immune function.

In this report we review our hypotheses and approaches to the study of the relationship between the central nervous and immune systems. Discussed are results pertaining to the modulation of immune parameters resulting from perturbations of the brain employing electrolytic lesions and the neuroleptic 6-hydroxydopamine. Experiments describing the central and peripheral effects of serotonin on in vivo and in vitro immune responses are also discussed.

Animals↗
PubMed1974

Pathogenesis of rinderpest virus infection in rabbits. II. Effect of rinderpest virus on the immune functions of rabbits.

Rinderpest virus infection was shown to induce marked suppression of both humoral antibody response and cell-mediated immunity in rabbits. The virus exhibited a suppressive effect on primary antibody response as indicated by a decrease in numbers of plaque-forming cells (immunoglobulin [Ig]M) and hemagglutinating antibody titers of both IgM and IgG types to sheep red blood cells, whereas there was no detectable effect of the virus on the production of memory cells. Virus-induced suppression of cell-mediated immunity was demonstrated by a decreased rate of proliferative response of peripheral lymphocytes to phytohemagglutinin stimulus and by a depression of delayed-type skin reactions to purified protein derivative. Such suppressive effects were indicated to persist for 14 days or longer. Alteration in phagocytic activity of the reticuloendothelial system was not observed. The relevance of the virus-induced histological lesions in the lymphoid tissues to the virus-induced immunosuppression was discussed.

Animals↗
PubMed1996

Immune functions and immunopathology of the mucosa of the upper respiratory pathways.

The specific defence of airway mucosae depends primarily on secretory immunity. The B cells involved are initially stimulated in organized mucosa-associated lymphoid tissue, apparently including the tonsils and adenoid. From these inductive sites, memory cells migrate to secretory effector sites where they differentiate terminally to immunoglobulin (Ig)-producing plasma cells. Locally produced Ig consists mainly of J chain-containing dimers and larger polymers of IgA (pIgA) that are selectively transported through glandular cells by an epithelial receptor called secretory component or the pIg receptor. IgG can participate in immune exclusion because it reaches the secretions by passive diffusion. However, its proinflammatory properties render IgG antibodies of local immunopathological importance when elimination of penetrating antigens is unsuccessful. T helper (Th) cells activated in this process may by a Th2 cytokine profile promote persistent inflammation with extravasation and priming of eosinophils. This development appears to be part of the late-phase allergic reaction, perhaps initially driven by interleukin-4 (IL-4) released from mast cells that are subjected to IgE-mediated activation, and subsequently also by Th2 cell activation. Eosinophils are potentially tissue-damaging, particularly after priming with IL-5. Various cytokines up-regulate adhesion molecules on endothelial and epithelial cells, thereby enhancing migration of eosinophils into the mucosa, and perhaps in addition causing aberrant immune regulation within the epithelium. Soluble antigens bombarding the epithelial surfaces normally seem to induce several immunosuppressive mechanisms, but mucosal homeostasis appears less patent in the airways than oral tolerance to dietary antigens operating in the gut.

B-Lymphocytes↗