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Results for “Immune function”

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PubMed2004

Regulators of G protein signaling: potential drug targets for controlling cardiovascular and immune function.

Heterotrimeric G-protein-coupled receptors (GPCRs) mediate a wide variety of organismal functions ranging from vision, olfaction, and gustation to the development and physiology of the cardiovascular, neuronal, and immune system. Naturally they are targets of a large number of therapeutic drugs. The regulators of G protein signaling (RGS) are a family of diverse proteins that regulate the GPCR-mediated signaling pathways principally by acting as GTPase activating proteins (GAPs) for the alpha subunit of the heterotrimeric G-proteins. Certain members of the RGS family contain multiple domains and motifs that mediate interactions with other signaling molecules, thus linking GPCR-dependent and GPCR-independent signaling pathways. Because of their ability to fine-tune vital GPCR-mediated processes and recent findings linking them to brain disorders, retinitis pigmentosa, and cancer RGS proteins have become excellent candidates for new drug discovery. The focus of this review is to discuss the roles of the RGS proteins in the development and normal physiology of cardiovascular and immune system, and to explore their potential as drug targets useful for the treatment of pathological conditions of the cardiovascular and immune systems.

Animals↗
PubMed2004

Evidence for potential mechanisms for the effect of conjugated linoleic acid on tumor metabolism and immune function: lessons from n-3 fatty acids.

Conjugated linoleic acid (CLA) and the long-chain polyunsaturated n-3 fatty acids have been shown in vivo and in vitro to reduce tumor growth. Tumor growth could occur by slowing or stopping cell replication (by interfering with transition through the cell cycle), increasing cell death (via necrosis and/or apoptosis), or both. The anticancer effects of fatty acids, shown in vivo, could also be mediated by effects on the host's immune system. Although it is widely recognized that n-3 fatty acids can alter immune and inflammatory responses, considerably less is known about CLA. For n-3 fatty acids, several candidate mechanisms have been proposed for their immune effects, including changes in 1) membrane structure and composition, 2) membrane-mediated functions and signals (eg, proteins, eicosanoids), 3) gene expression, and 4) immune development. Considerable work has been done that shows the potential importance of CLA as an anticancer treatment; however, many questions remain as to how this effect occurs. This review summarizes the CLA and cancer literature and then uses the evidence for the anticancer immune and tumor properties of the long-chain n-3 fatty acids docosahexaenoic and eicosapentaenoic acids to suggest future research directions for mechanistic studies on CLA and cancer.

Animals↗
PubMed2005

Immune function of C1q and its modulators CD91 and CD93.

C1q is a subcomponent of the first component of complement C1, which is a multimolecular complex comprising one molecule of C1q and two molecules each of the autoreactive proteases, C1r and C1s. This multimolecular complex triggers the classical pathway of complement. Advances in the past several years have provided a partial crystal structure of the C1q subunit. This, together with gene deletion of C1q, has allowed further insight into the multifunctional immune aspects of this molecule. Two C1q-mediated functions that have received intense scrutiny recently are C1q-mediated apoptotic clearance of cell debris and phagocytosis. This has led to a heightened search for specific receptors for the collagen-like region (CLR) as well as the globular heads. Two transmembrane proteins, CD91 and CD93, have been proposed to interact indirectly with the CLR of C1q, promoting apoptotic clearance and phagocytosis, respectively. The aim of this article is to provide an overview of the structural and functional information that implicates CD91 and CD93 in C1q-mediated functional effects.

Animals↗
PubMed1997

Housing and exercise of dogs: effects on behavior, immune function, and cortisol concentration.

We examined the effect of supplemental exercise (either individually or with a conspecific) on the physical and psychological health of dogs by measuring immune, endocrine, and behavioral responses. Forty purpose-bred adult male beagles were assigned to one of four treatment conditions: exercised individually (EI), exercised with a conspecific (EC), nonexercised (NE), or cage control (CC). Each EI dog was removed from its cage, carried to an empty room, and allowed to exercise alone for 20 min/d 3 days a weeks for 12 weeks. Two EC dogs were allowed to exercise together following a similar schedule. To control for potential handling effects, NE dogs were removed from their cages, carried to the exercise room, but immediately returned to their cages, and CC dogs remained in their cages during scheduled exercise periods. Detailed behavioral observations, humoral immune responses to the antigen keyhole-limpet hemocyanin, peripheral blood mononuclear cell subsets, plasma cortisol concentration, body weight, and total and differential white blood cell (WBC) counts were routinely monitored. Results indicated few significant treatment effects on physiologic or behavioral measures. Specifically, EC dogs had lower percentages of B lymphocytes, and EC and EI dogs barked more than did NE or CC dogs. However, some physiologic and behavioral measures changed as a function of time regardless of treatment condition. Most notably, for all dogs over time, WBC counts, plasma cortisol values, and behavioral measures reflecting inactivity decreased, while measures reflecting high activity and abnormal behaviors increased. We concluded that neither exercise treatment substantially altered the physical health of research dogs, and perhaps more importantly, failed to prevent the development of abnormal behavior.

Animal Husbandry↗
PubMed1997

Clues to immune function and oncogenesis provided by events that activate the cell cycle machinery in normal human T cells.

A common feature seen in states of decreased immune competence or immunosuppression and in diseases of the blood, such as lymphohematopoietic cancers, is the disruption of the normal pathways of cell cycle control. In lymphocytes a series of nonlinear biochemical cascades leads to cellular proliferation and also controls the production of cytokines that provide immunologic help (i.e., aid in B and T cell proliferation, maturation, and differentiation). These two distinct outcomes can be dissociated, as stimuli that incite production of cytokines need not lead to cell division, and conversely, exogenously provided cytokines may promote lymphocyte proliferation. The signals that induce production of cytokines, particularly interleukin-2, have been extensively characterized. It also is known that the fidelity of cell cycle progression is dependent on a regulatory network whose key components include cyclin-dependent kinases and cyclins. This review describes the current state of knowledge linking the antigen receptor response pathways and the activation of the cell cycle machinery in T cells.

Animals↗
PubMed1999

Green fluorescent protein-transgenic mice: immune functions and their application to studies of lymphocyte development.

Green fluorescent protein (GFP) transgenic (GFP+) mice express GFP in most tissues except erythrocytes and hair. Immune responses of GFP+ mouse and their application to studies of lymphocyte development were investigated. Flow cytometric analyses revealed that differentiation patterns of lymphocytes from GFP+ mice are equivalent to those from parental C57BL/6 mice. There was no difference in mature T-cell proliferative ability in response to allogeneic stimulator cells or anti-CD3epsilon stimulation between GFP+ and C57BL/6 mice. Furthermore, the anti-OVA antibody response of GFP+ mice was also the same as that of C57BL/6 mice. Taken together, these results show no immunological differences between GFP+ and C57BL/6 mice. Bone marrow transplantation and in vitro thymus reconstitution experiments were performed in an attempt to apply the GFP+ mice to the analysis of lymphocyte development. When bone marrow cells from GFP+ mice were transplanted. T and B lymphocytes containing GFP developed normally in scid recipients. Next we examined intrathymic T-cell development by hanging drop culture methods. GFP+ and CD4+8+ immature T-cells developed normally from bone marrow cells in the reconstituted thymus. The experimental system using hematopoietic cells from GFP+ mice is a powerful tool for visualizing lymphocyte development.

Animals↗
PubMed2003

[Cellular and molecular mechanisms of regulation of immune functions by catecholamines].

An increasing body of evidence suggests that catecholamines (CAs) do not only cause a general immunosuppression as previously believed, but suppress cellular immunity and boost humoral response. CAs can inhibit T helper 1 cells, T cytotoxic cells, natural killer cells and monocytes, but enhance T helper 2 cells and B cells through their direct regulation of these immune cells. In addition, CAs may modulate the gene transcription for cytokines in immune cells through stimulation of beta 2-adrenoreceptors and increase of cAMP, subsequently, activation of protein kinase A and alteration of the activity of nuclear transcription factors. Through these molecular mechanisms, the production of interleukin-2 (IL-2), tumor necrosis factor-alpha and IL-12 is decreased, but the production of IL-6, IL-10 and IL-4 is increased.

Animals↗
PubMed1992

Opiates and immune function. Consequences on infectious diseases with special reference to AIDS.

There is an increasingly body of evidence, obtained both in vitro and in vivo, showing that exogenous opioids have a variety of effects on cells of the immune system. The consequence is that opiates at pharmacological concentrations suppress cell-mediated immunity, as reflected by depressed T-dependent antibody production by B lymphocytes, altered T lymphocyte functions such as proliferation, delayed-type hypersensitivity, graft-versus-host responses and decreased cytotoxic NK cell activity. The macrophage/monocyte oxidative burst and phagocytosis are also impaired, effects probably mediated by various opioid receptor types as they are blocked or reversed by naloxone, an opioid antagonist. Other possible mechanisms of interaction remain to be elucidated: exogenous opioids can act on neurons of the central nervous system, thereby activating the neuroendocrine system with a subsequent increase in serum glucocorticoid levels. Another potential link between the central nervous system and lymphoid tissue is the sympathetic nervous system, via which opioid-induced activation could result in noradrenergic inhibition of the immune system. The clinical consequences of these suppressive effects on the immune system are seen in the striking increase in the incidence of infections in intravenous opioid addicts. The advent of AIDS and the identification of intravenous drug abusers as a critical risk group have propelled interest in this area. Data obtained both in vitro and in vivo with various experimental models shows that morphine increases susceptibility to bacterial and viral infections, the latter effect possibly being related to a depressive effect of opioids on gamma-interferon levels. The dosage and time of administration strongly influence the results: it appears that chronic opioid treatment in vivo induces a state of immune tolerance, with normal resistance to viral infections, whereas short or single administration has a detrimental effect. In the former context, other factors such as a morphine-induced increase in CD4+ cell numbers may tend to enhance the infectivity of HIV-infected subjects.

AIDS-Related Opportunistic Infections↗
PubMed1991

Aging and immune function.

Since it is too difficult to study aging of the organism as a whole, most investigators try to focus on a specific physiological system that exhibits age-dependent functional changes, in the hopes that elucidation (in biochemical and developmental terms) of the mechanism of senescent change will provide insight into the aging process itself. The immune system is among the most maleable of such models, in that well-defined cell types will produce well-defined molecules with predictable functions in vitro and in vivo. The increasing power of basic immunological science should, in the next decade, permit an increasingly fine appreciation of how aging leads to immune decline. This expanding conceptual framework will then suggest new ideas about the role of immunosenescence in degenerative, infectious, and neoplastic illnesses and may also generate increasingly rational strategies for therapeutic intervention.

Aging↗
PubMed2006

Inflammatory mediators and immune function are altered in home parenteral nutrition patients.

OBJECTIVES: Patients who used home parenteral nutrition (HPN) and healthy, volunteer control subjects were examined to assess relative immune potential and inflammatory marker expression and to investigate the association between HPN and immune parameters. METHODS: Subjective Global Assessments were performed on all subjects. The peripheral blood concentration of C-reactive protein was determined by enzyme-linked immunosorbent assay. The peripheral blood concentration of systemic inflammatory mediators that included tumor necrosis factor-alpha (TNF-alpha), soluble TNF-alpha receptors p55 and p75, and interleukin-6 were similarly determined. Peripheral blood lymphocytes were isolated and the percentage of circulating CD4+ and CD8+ lymphocytes was determined by flow cytometry. In addition, peripheral blood lymphocytes were cultured in the presence of the T-cell mitogen, phytohemagglutinin, and the proliferative response of the CD3+ population was assessed by flow cytometry. Results of these experiments were obtained for 10 clinically stable patients who had used HPN longer than 2 y and these results were compared by Student's t test with data obtained for 12 normal, volunteer control subjects. RESULTS: Of the 10 patients who used HPN and were examined, seven had short bowel syndrome, two had dysmotility, and one required HPN due to radiation enteritis. Based on Subjective Global Assessments, all patients were well nourished. No difference was observed in TNF-alpha level between groups and C-reactive protein levels were within normal limits (1.2 mg/L in patients, 0.99 mg/L in controls). Soluble TNF-alpha receptors p55 and p75 were significantly increased (P < 0.001), but serum interleukin-6 was not (P = 0.07). The percentage of CD8+ cells and the CD4+/CD8+ ratio were not statistically different between groups. In contrast to this result, the percentage of CD4+ cells and the proliferative T-cell response to phytohemagglutinin were significantly depressed in patients who used HPN versus control subjects. CONCLUSIONS: These data suggest the presence of an underlying inflammatory process and subsequent abnormal T-lymphocyte function in patients who use HPN.

Adolescent↗
PubMed2006

Use of an immune function assay to monitor immunosuppression for treatment of post-transplant lymphoproliferative disorder.

The first-line treatment for PTLD is reduction in immunosuppression, allowing partial reconstitution of cell-mediated immunity. However, there is a risk of inducing acute allograft rejection during clinical resolution of PTLD. A recently available assay, Immuknow, measures the cell-mediated immune response and could be used to monitor reduction of immunosuppression. We report a case of PTLD occurring in a pediatric kidney transplant recipient where the reduction in immunosuppression was serially followed using this assay and quantitative EBV-PCR. A rapid reduction to minimal immunosuppression was followed by resolution of PTLD. Later, when the cell-mediated immune response increased, with negative viral load, immunosuppression was gradually increased utilizing the assay to adjust dosing. Presently, there are no signs of PTLD and renal function remains normal.

Child, Preschool↗