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Query: UMLS:C0009450 (infectious diseases)
 83,438 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent advances in cellular and molecular biology have allowed investigators to better understand the mechanisms of inflammatory and immune responses in many infectious diseases. Soluble mediators produced by various inflammatory and structural cells, collectively called cytokines, have been shown to play a crucial role in the pathogenesis of most of these diseases, including periodontal disease. This paper globally reviews recently reported findings implicating cytokines in periodontal pathophysiology. Inflammatory mediators, such as interleukin-1, tumor necrosis factor-alpha, and interferon-gamma, known to regulate bone resorptive activity are present in diseased periodontal tissues. Similarly, metalloproteinases, which degrade extracellular matrix, have been shown to have increased activity in diseased sites, and enhanced levels of their inhibitors correlate with absence of disease activity. Finally, certain polypeptide growth factors originally known to play a role in wound healing are now shown to have a significant effect in inflammatory responses.
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PMID:The role of cytokines in the pathogenesis of periodontal disease. 803 65

We here describe an efficient procedure for overexpression and purification of recombinant complete human interferon-gamma (IFN-gamma) receptor (IFN-gamma-R) and its extracellular fragment employing a baculovirus (BV) expression system. Infection of Sf 158 cells with recombinant BV results in membrane expression of high affinity IFN-gamma-R (Kd 1.6 x 10(-10) M), with approximately 10(6) molecules/cell 40 h postinfection. Solubilized, affinity-purified IFN-gamma-R and a secreted extracellular domain of IFN-gamma-R were compared for ligand-binding capacity and antagonistic activity in an IFN-gamma bioassay. Our results show that the complete receptor has a 2.5-fold higher ligand affinity and a 15-fold higher IFN-gamma in vitro-neutralizing capacity in an in vitro virus protection assay as compared to the extracellular fragment. This suggests that the transmembrane and cytoplasmic domains of IFN-gamma-R contribute to stability and/or enhance formation of biologically active receptor complexes in solution.
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PMID:Expression of complete human IFN-gamma receptor and its extracellular domain in insect cells: purification and characterization of the recombinant proteins. 806 Nov 16

In addition to CD4, the primary receptor to which the human immunodeficiency virus type 1 (HIV-1) binds, mononuclear phagocytes (monocytes) express three classes of Fc receptors for immunoglobulin G (Fc gamma R). We have previously shown that infection of monocytes by HIV-1 is inhibited when bispecific antibodies (BsAbs) are used to target the virus to either the type I, type II, or type III Fc gamma R on these cells. Infection of monocytes was not inhibited when HIV-1 was targeted to either human leukocyte antigen class I or CD33. We have extended these studies to examine the ability of BsAbs plus polymorphonuclear leukocytes (neutrophils, PMNs) and monocytes to reduce infectivity of HIV-1 to cells from the human T cell lymphoma line, H9. The production of HIV-1 following interaction of virus with BsAb and phagocytes was determined in an indicator cell assay by mixing BsAb, HIV-1, and phagocytes with uninfected H9 cells. Productive infection of H9 cells was quantitated on subsequent days by measuring p24 gag antigen levels in supernatants by enzyme-linked immunosorbent assay. Our findings show that the addition of interferon-gamma-activated PMNs or monocytes to cultures of HIV-1 plus H9 cells in the absence of BsAb results in a marked reduction in p24 levels equivalent to 85 to 90% of control levels. With the combination of BsAb (anti-Fc gamma RI x anti-gp120) plus IFN-gamma-activated phagocytes, levels of p24 in H9 cultures were below those at culture initiation. These findings demonstrate that IFN-gamma-activated phagocytes can affect the natural course of HIV-1 infection of T cells, a finding of potential clinical importance.
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PMID:Targeting HIV-1 to Fc gamma R on human phagocytes via bispecific antibodies reduces infectivity of HIV-1 to T cells. 812 Apr 55

Eight adult patients with visceral leishmaniasis acquired in mediterranean countries were treated in a prospective study with a combined immunomodulating and antiparasitic regimen consisting of low-dose interferon-gamma (IFN-gamma) and pentavalent antimony. The clinical outcome, hematological and parasitological parameters, the duration of treatment and number of treatment cycles as well as the cumulative dose of pentavalent antimony applied, have been evaluated. The combined treatment led to complete resolution of symptoms and parasitological cure in all cases of visceral leishmaniasis without major side effects. Combined treatment resulted in a significant reduction of duration of treatment (19 vs. 31 days, p < 0.02) and cumulative dose of pentavalent antimony (11.67 vs. 19.30 g, p < 0.02) compared to historical controls (n = 6). No relapses occurred after a median follow-up of 9 months (range: 2-28 months). We conclude that combination therapy is tolerated well and is highly effective in patients with visceral leishmaniasis. The addition of IFN-gamma to standard therapy with pentavalent antimony may reduce the cumulative dose of antimonial drugs, shortens the treatment period and probably reduces the number of relapses.
Infection
PMID:Short term treatment of visceral leishmaniasis of the Old World with low dose interferon gamma and pentavalent antimony. 813 64

The cerebral endothelial cell line, 33-Mse, was characterized for its MHC antigen expression, infectability with viruses and capacity to present antigen to immune spleen cells. The cell line had interferon-gamma inducible MHC antigen expression. Infection by Theiler's murine encephalomyelitis influenced the expression of MHC molecules on the cell surface of this line. These cells could not stimulate T splenocyte proliferation or act as targets for Theiler's murine encephalomyelitis cytolytic immune spleen cells. These cells were able to present viral antigen to vaccinia virus immune spleen cells and act as targets for cytotoxic T cells from vaccinia virus immune mice.
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PMID:Characterization of a murine central nervous system-derived cell line: infectability and presentation of viral antigen. 815 35

Cytokines are key mediators of the immune system, dictating the quality of the host response to infection. The importance of such immune mediators to the development of immune and inflammatory responses has emerged from work in mouse and man, however it has now become necessary to produce the equivalent (and novel) cytokines in ruminants. Over the past three years recombinant DNA techniques have allowed the cloning of numerous ovine cytokines. These include interleukins -1, -2 and -3 (IL-1, -2 and -3), interferon-gamma (IFN-gamma), ovine trophoblast protein (oTP-1), tumour necrosis factor-alpha (TNF-alpha) and granulocyte-macrophage colony-stimulating factor (GM-CSF). The predicted amino-acid sequences of these ovine proteins show varying degrees of similarity with the equivalent human proteins thus explaining why some of the cytokines are not biologically cross-reactive between species. Recombinant ovine proteins have been produced for IFN-gamma, oTP-1, IL-1, IL-3 and GM-CSF. Their biological activities are very similar to those of their human counterparts. Although it is too early to tell whether the recombinant ovine proteins will be of use in the treatment or prophylaxis of infectious disease, work in cattle and pigs has indicated the potential usefulness of cytokines in this role.
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PMID:Current research on ovine cytokines. 822 Oct 42

Patients rendered T cell-deficient by advanced disease due to human immunodeficiency virus, an underlying neoplastic disorder, or immunosuppressive therapy are vulnerable to a select group of opportunistic infections. These infections, which often fail to respond to conventional therapy, provide the clinical setting in which the efficacy of treatment with cytokines can be tested. Particularly pertinent cytokines are those that activate macrophages and monocytes or enhance T-cell function. Experimental observations and emerging data from patients with intact T-cell function suggest that treatment with at least three cytokines, interferon-gamma, interleukin-2, and granulocyte-macrophage colony-stimulating factor (GM-CSF) may be of benefit. Each of these cytokines is already in clinical use, and each has therapeutic potential in a variety of different infectious disease. Patients with infections caused by opportunistic intracellular pathogens appear to be the most appropriate candidates for adjunctive cytokine therapy.
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PMID:Cytokines as antimicrobial therapy for the T cell-deficient patient: prospects for treatment of nonviral opportunistic infections. 827 6

Expression of either the CD4 or CD8 glycoproteins discriminates two functionally distinct lineages of T lymphocytes. A null mutation in the gene encoding CD4 impairs the development of the helper cell lineage that is normally defined by CD4 expression. Infection of CD4-null mice with Leishmania has revealed a population of functional helper T cells that develops despite the absence of CD4. These CD8- alpha beta T cell receptor+ T cells are major histocompatibility complex class II-restricted and produce interferon-gamma when challenged with parasite antigens. These results indicate that T lymphocyte lineage commitment and peripheral function need not depend on the function of CD4.
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PMID:Helper T cells without CD4: control of leishmaniasis in CD4-deficient mice. 836 26

Despite the importance of tuberculosis as the leading cause of death due to infectious disease in the world, it has only been recently that an understanding of the human host response in this infection has begun to emerge. The key components of this response are cytokines and components of cellular immunity, predominantly T-lymphocytes and macrophages. Though the relationships among the components of the immune response are complex, it seems likely that in response to mycobacterial infection associated with active disease, cytokines such as TNF-alpha and IL-1 beta are produced; these cytokines serve to recruit more lymphocytes, generally of the T(H) (T helper) phenotype, which then produces substances such as the macrophage activating factor interferon-gamma. Macrophages activated by IFN-gamma ar thus stimulating to enhance intracellular killing of mycobacteria. The role of other cytokines, such as IL-6 and IL-8, both of which are induced by M. tuberculosis or its cell was components, is less clear. Further elucidation of the human host response to tuberculosis should help in the development of new vaccines and treatment strategies.
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PMID:Human host response to Mycobacterium tuberculosis. 852 36

The infectious disease background and particularly the helminth infections that are endemic in Africa could have profound effects on the host immune system. Studies that we have performed on an Ethiopian HIV- immigrant population that has recently reached Israel, lend support to this notion. They have indeed revealed a very high prevalence of helminth and several other infections with an extreme immune dysregulation, consisting of: (i) highly elevated plasma IgE, IgG, placental isoferritin, p75 soluble TNF receptor (sTNFR) levels and very high blood eosinophilia; (ii) increased secretion from phytohaemagglutinin (PHA)-simulated peripheral blood mononuclear cells (PBMC) of the cytokines IL-2, IL-4, IL-10 and p75 sTNFR, and decreased secretion of interferon-gamma (IFN-gamma) and IL-6; (iii) increased and decreased surface expression of p75 TNFR and IL-6 receptor on lymphocytes, respectively. The causal relationship between this immune dysregulation and the infectious background is highly suggestive, and could have far-reaching implications in the resistance to other infections.
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PMID:Immune dysregulation in Ethiopian immigrants in Israel: relevance to helminth infections? 856 6


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