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PubMed2003

Doxorubicin induces specific immune functions and cytokine expression in peritoneal cells.

To examine the basis of the immune modulation induced by the anticancer agent doxorubicin (DOX), the immunophenotype, tumoricidal activity, cytokine protein and mRNA expression were determined using peritoneal exudate cells (PEC) from saline-treated (untreated) and DOX-treated mice. A greater percentage of PEC from DOX-treated mice than from untreated mice were adherent to plastic, had characteristics of granulocytes, and were positive for the NK1.1, CD11b/Mac-1, and CD3 markers. DOX decreased the percentage of CD45R/B220+ cells. PEC from DOX-treated mice had greater tumoricidal potential than those from untreated mice since IL2, LPS, or IFNgamma alone increased the cytolytic activity of PEC from DOX-treated mice, whereas PEC from untreated mice required both LPS and IFNgamma to become cytolytic. DOX treatment modulated the expression of specific cytokines. Following stimulation in culture, PEC from DOX-treated mice produced more TNF, IL1, and IFNgamma than PEC from untreated mice. DOX treatment increased the levels of TNF, but not IL1, mRNA and decreased the levels of IL6 mRNA and protein. These data demonstrate that a single DOX injection induces specific effects in PEC and, as a consequence, increases the tumoricidal potential of cells of the macrophage and natural killer types.

Animals↗

PubMed2001

Obsessive compulsive disorder: is there an association with childhood streptococcal infections and altered immune function?

During the last few years, an increased interest in the possibility of immune mediated pathophysiology of obsessive compulsive disorder (OCD) and related disorders has been seen. In the late 1980s, the National Institute of Mental Health reported an increase of obsessive compulsive symptoms in patients with Sydenham chorea (SC). Subsequently, a precipitating streptococcal infection in children with sudden onset of OCD symptoms but no chorea led to the coining of PANDAS (pediatric autoimmune neuropsychiatric disorders associated with streptococcus). This association has furthered interest in studying immune parameters in non-PANDAS OCD as well. This article will review the neuropsychiatric findings in OCD and Tourette syndrome (TS) with emphasis placed on PANDAS, and its association with SC, and a review of the existing studies that have assessed immunologic measures in patients with OCD and TS.

Adult↗

PubMed2001

Anti-inflammatory effects of theophylline: modulation of immune functions during murine leukemia virus infection.

LP-BM5 murine leukemia virus induces immune dysfunction leading to B cell leukemia and murine AIDS with cytokine dsyregulation. Theophylline induces apoptosis of leukemia cells in humans. Therefore the effects of theophylline on immune dysfunction in a murine model of leukemia were investigated. C57BL/6 mice consumed drinking water containing 0.3% theophylline beginning 2 weeks after murine retrovirus infection for 4 months. Theophylline largely prevented the retrovirus induced splenomagaly, lymphodenopathy, reduction in B and T cell proliferation, and suppression of Thl cytokines (IL-2) secretion. It also suppressed Th2 cytokine (IL-4, TNF-alpha, and IL-10) production, which was otherwise stimulated by retrovirus infection. These data suggest that immune dysfunction, induced by murine retrovirus infection, was largely prevented by theophylline treatment.

Animals↗

PubMed1994

Effect of the administration of growth-hormone-producing lymphocytes on weight gain and immune function in dwarf mice.

Our previous work has shown that cells of the immune system produce a growth hormone (GH) molecule similar to that secreted by the pituitary. In the present studies, we evaluated the possibility that normal spleen cells producing GH transferred to dwarf mice could stimulate their growth. The results showed that normal spleen cells alone or spleen cells treated with growth-hormone-releasing hormone (GHRH) did not appear to significantly stimulate the growth of dwarf mice. Spleen cells activated in vitro with concanavalin A or lipopolysaccharide and then transferred to dwarf mice, or thymus cells alone, were also without effect, whereas GH alone stimulated growth as expected. Serum levels of insulin-like growth factor-I (IGF-I) and IGF-I-liver RNA were undetectable in control dwarf mice and dwarf mice receiving spleen cells, whereas serum levels of IGF-I increased after treatment of dwarf mice with GH. The immune system of dwarf mice receiving spleen cells, however, was significantly altered. Spleen cells from dwarf animals showed enhanced immunoglobulin, interleukin (IL)-6, IL-2, and interferon-gamma production whereas no significant change was apparent in natural killer cell activity. Despite the absence of the pit-1 protein in dwarf mice, their spleen and thymus cells retained the ability to produce almost as much lymphocyte GH as normal. Overall, the findings support the idea that the pit-1 protein in lymphocytes of dwarf mice may not be obligatory for the expression of lymphocyte GH.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2004

Thematic review series: the immune system and atherogenesis. Immune function in atherogenesis.

In this overview to a new thematic series on the immune system and atherogenesis, I provide a very brief summary of current conceptions of atherogenesis, of the innate and adaptive immune systems, and of the participation of the latter in atherogenesis, with particular emphasis on studies of the involvement of the immune system in atherosclerosis reported in the last 2 years. This is followed by a short outline of the eight reviews that will make up this thematic series. The overview is concluded with some caveats that should be considered in the analysis of atherosclerosis in experimental animals.

Animals↗

PubMed1982

Immune function in patients with chromosome deletions.

Non-specific, cell-mediated and humoral immunity were evaluated in six patients with different autosomal deletions, and in two patients with X-chromosome deletions. Six had an increased number of bacterial, viral, and mycotic infections. Mild disturbances were found in the immunological functions of almost every patient. Granulocyte phagocytosis and killing of bacteria were normal in all patients. The chemotactic response was increased in two, and normal in the others. The responses to phytohaemagglutinin and pokeweed mitogen were normal in all patients and the response to concanavalin A was decreased in one patient. The lymphocyte response to purified protein derivative was decreased in the patients as a group when compared to the controls (P less than 0 . 005), but normal to oidiomycin. The number of acid-alpha-naphthyl acetate esterase positive cells was low in four patients. One had a high titre of antinuclear and antithyroid antibodies. One had a low concentration of serum IgA, C3 and C4. One had a high concentration of IgM. Two had elevated levels of C3 and C4. Our results show that several different chromosomal deletions are associated with immunological abnormality.

Adult↗

PubMed1998

Regulation of the cAMP cascade, gene expression and immune function by cannabinoid receptors.

The objective of this article is to discuss the putative role of cannabinoid receptors in immune modulation by cannabinoid compounds. The primary focus is on the signal transduction events that are initiated following ligand binding to cannabinoid receptors and how these events lead to detrimental effects on the normal responsiveness of immunocompetent cells. Toward this end, signalling events are traced from the cannabinoid receptor to the transcription factors which are adversely regulated in the presence of cannabinoid compounds during leukocyte activation. Moreover, this aberrant regulation of transcription factors is discussed in the context of altered gene expression and the impact this has on leukocyte function. Lastly, an important goal of this article is to dispel a long standing myth that the cyclic adenosine 3':5'-monophosphate (cAMP) cascade is a negative regulatory pathway for immunocompetent cells. This chapter examines two major immunologic cell-types which are well established as exhibiting altered function following cannabinoid treatment, helper T-cells and the macrophage. Not discussed are the effects of cannabinoids on B-cell function. This is primarily due to the rather refractory nature of B-cells to inhibition by cannabinoids in spite of the fact that this cell-type expresses functional cannabinoid receptors [Schatz, A.R., Koh, W.S., Kaminski, N.E., 1993. Delta9-tetrahydrocannabinol selectively inhibits T-cell dependent humoral immune responses through direct inhibition of accessory T-cell function. Immunopharmacol., 26, pp. 129-137.]. One cautionary note, although the focus of this article is on cannabinoid receptor mediated signalling events, immune modulation by cannabinoid compounds is likely multi-factorial presumably involving receptor as well as receptor-nonrelated events. Effects on leukocytes by cannabinoids which are believed to be mediated by receptor-nonrelated events are outside the scope of this paper and will not be discussed. One last introductory point is that even though their is presumably little overlap in the genes which are regulated by cannabinoids in leukocytes as compared to other cell-types (e.g., neural cells), the major signalling pathways involved in cellular regulation are ubiquitous. With that in mind, it is likely that their is a considerable amount of similarity in the signalling pathways regulated by cannabinoids in cell-types of different lineage, given that they express cannabinoid receptors. In this context, signalling events observed in leukocytes can provide important insight into which genes may be modulated by cannabinoid in other cell types.

Animals↗

PubMed1976

HLA factors and immune function.

The HLA system is the major histocompatibility system (MHS) in man and contains a variety of closely linked genes, which control a large number of alloantigens, some complement components, and certain immune responses. The alloantigens are of three different kinds: (i) so-called "classical" or serologically detectable (SD) antigens which are present on all nucleated cells and controlled by genes of at least three different loci; (ii) MLC (= mixed lymphocyte culture = LD = lymphocyte dependent) antigens which are as yet only recognizable by in vitro culture assays; (iii) Ia (= immune-associated) antigens which (like MLC antigens) primarily are present on B lymphocytes and which can be detected serologically. Our knowledge of immune-response (Ir) determinants in man is as yet rather limited but by inference from studies of MHS in mice, guinea-pigs, and rhesus monkeys it is almost certain that HLA contains such genes. Immune response genes control in a dominant way the ability to respond specifically with IgG antibody production and cell-mediated immunity to certain specific antigens. Ir genes are closely linked to the MLC and Ia genes. They seem to be particularly important for immune responses involving T lymphocyte function (including T-B cell cooperation), and it seems likely that they code for "antibody-like", carrier-specific immune receptors on T cells. Evidence that HLA contains Ir determinants derives from the observations (i) that a variety of "immunopathic" disorders are associated with HLA factors; (ii) that ragweed hayfever seems to be inherited with certain HLA types within families; and (iii) that the occurrence of anti-adrenal antibodies is associated with HLA in Addison's disease. Autoimmune thyreoiditis is controlled by the MHS in mice and chickens, and in analogy, Graves' disease is associated with HLA in man.

Autoantibodies↗

PubMedDate not supplied

Genetic dissection of age-related changes of immune function in mice.

Understanding of the genetic basis of normal and abnormal development of the immune response is an enormous undertaking. The immune response, at the most minimal level, involves interactions of antigen presenting cells (APCs), T and B cells. Each of these cells produce cell surface and soluble factors (cytokines) that affect both autocrine and paracrine functions. A second level of complexity needs to consider the development of the macrophage/monocyte lineage as well as the production of the common lymphoid precursor which undergoes distinct maturation steps in the thymus and periphery to form mature T cells as well as in BM (BM) and lymphoid organs to form mature B cells. A third level of complexity involves the immune response to infectious agents including viruses and also the response to tumour antigens. In addition, there are imbalances that predispose to decreased responses (immunodeficiencies) or increased responses (autoimmunity). A fourth level of complexity involves attempts to understand the differences in the immune response that occurs at a very young age, in adults, and at a very old age. This review will focus on the use of C57BL/6 J X DBA/2 J (BXD) recombinant inbred (RI) strains of mice to map genetic loci associated with the production of lymphoid precursors in the BM, development of T cells in the thymus, and T-cell responses to stimulation in the peripheral lymphoid organs in adult and in aged mice. Strategies to improve the power and precision in which complex traits such as the age-related immune response can be mapped is limited with the current set of 35 strains of BXD mice. Strategies to increase these strains by generating recombinant intercross (RIX) strains of mice are being developed to enable this large set of lines to detect quantitative trait loci (QTLs) with a much higher consistency and statistical power. More importantly, the resolution with which these QTLs can be mapped would be greatly improved and, in many cases, adequate to carry out direct identification of candidate genes. It is likely that, given the complexity of the immune system development, the number of cells involved in an immune response, and especially the changes in the immune system with ageing, mapping hundreds of genes will be required to fully understand age-related changes in the immune response. This review outlines ongoing and future strategies that will enable the mapping and identification of these genes.

Aging↗

PubMed1980