UMLS:C0153470 - FACTA Search

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Query: UMLS:C0153470 (Spleen)
4,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The in vitro effects of cocaine on antigen-specific-induced cytokine production by murine splenocytes was evaluated both by quantitation by ELISA of the cytokines in culture supernatants and by flow cytometric analysis of the frequency of the cytokine-producing CD4+ T cells. Spleen cells from mice immunized with ovalbumin (OVA) were restimulated with OVA in the presence or absence of cocaine for different periods of time and then evaluated for production of cytokines. Exposure to cocaine was found to reduce the levels in culture supernatants of IL2 and IFN-gamma, whereas IL4 and IL5 levels were not changed. Flow cytometric analysis showed that cocaine increased the frequency of IL2- but not of IL4-producing CD4+ T cells. Kinetics studies indicated that the in vitro antigen-specific-induced production of IL2 is faster than that of IL4 and that cocaine did not affect the production kinetics of either cytokine. Collectively, the results suggest that in vitro cocaine acts by interfering with the secretion rather than with the synthesis of cytokines and that the drug exerts different effects on cytokines with different production kinetics.
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PMID:In vitro effects of cocaine on cytokine secretion induced in murine splenic CD4+ T cells by antigen-specific stimulation. 754 72

In a fully MHC plus multiple minor antigen-mismatched murine bone marrow transplantation (BMT) model, we have demonstrated that a short course of high dose IL-2, begun on the day of BMT, protects against graft-versus-host disease (GVHD). This inhibitory effect is directed against donor CD4+ cells. To determine whether the mechanism of IL-2-induced GVHD protection involves clonal deletion or anergy of host-reactive donor T helper cells (Th), we performed limiting dilution analyses to measure the frequency of activated Th that reacted to donor, host, and third-party antigens in GVHD control and IL-2-protected mice. Marked and specific expansion of host-reactive Th was observed to a similar extent in GVHD control and IL-2-protected mice by day 5 after BMT, and the number of these cells in the spleen increased by several orders of magnitude between days 3 and 5 after BMT, which suggests that recirculation from other tissues occurred in this period. A high proportion (approximately 80%) of donor T cells expressed CD25 in both GVHD control and IL-2-protected mice on day 4 after BMT, which suggests a high level of bystander T cell activation. Since marked quantitative differences in the GVH response were not observed between GVHD control and IL-2-protected mice, we assessed both groups for qualitative differences in the Th response. Spleen cells isolated in the first 8 days after BMT were cultured with host-type, donor-type, or third-party stimulators or without stimulators, and cytokines were measured in supernatants harvested at 24 hr. GVHD was associated with marked increases in supernatant IFN-gamma levels from day 3 to day 6 after BMT, and with increases in IL-2 levels compared with naive A/J controls or syngeneic BMT controls stimulated with host antigens. Production of these cytokines was specifically induced by host-type antigens. Supernatants from spleens of IL-2-treated mice showed delayed kinetics of IFN-gamma production, and tended to contain higher levels of IL-4 in response to host antigen compared with GVHD controls on days 2 and 4 after BMT. Both IL-4 and IFN-gamma were produced almost exclusively by CD4+ cells in spleens of GVHD control and IL-2-protected mice on day 4. However, no consistent difference was observed between the groups in supernatant IL-2 or IL-10 levels, ruling out a simple Th1 to Th2 switch.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Inhibition of graft-versus-host disease by interleukin-2 treatment is associated with altered cytokine production by expanded graft-versus-host-reactive CD4+ helper cells. 767 98

The present study was performed in order to define the responding populations and profiles of cytokine production in BCG-primed spleen cells restimulated in vitro with antigen. Spleen cells from DBA/2 mice, one of BCG-resistant strains (Bcgr), infected with Mycobacterium bovis BCG vigorously proliferated by restimulation with heat-killed BCG. This response peaked as early as on day 3 after BCG infection, and then decreased to the basal level by 3 weeks. Blocking of IL-2R alpha chain or IL-4 by each antibody partially inhibited it, but anti-IFN-gamma antibody did not, suggesting that both IL-2 and IL-4 were involved in the proliferation of primed spleen cells. CD4+ and gamma delta TCR-bearing T cell were responding populations to BCG, but CD8+ T cell was not, because depletion of CD4+ or gamma delta T cells by the treatment with each antibody and complement inhibited proliferation and IL-2/IL-4 production, but that of CD8+ T cells did not. Further study demonstrated that spleen cells from BCG-resistant DBA/2 mice produced more IL-2/IL-4 than those from BALB/c mice, one of BCG-susceptible strains (Bcgs), in response to BCG. These results suggest that both CD4+ and gamma delta TCR-bearing T cells play an important role in the host defense against M. bovis BCG infection, and that the magnitude of cytokine production is one of the critical factors to define the susceptibility of mice to this pathogen in the late phase of infection.
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PMID:[Analysis of antigen-specific proliferation and IL-2/IL-4 production of spleen cells from mice infected with Mycobacterium bovis BCG]. 776 May 38

Spleen cells from BALB/c mice bearing a syngeneic tumor (CSA1 M) 2 to 3 wk after inoculation with CSA1 M cells produced IL-2, IFN-gamma, and TNF upon in vitro cultures. This was previously demonstrated to be a result of collaboration between tumor-primed CD4+ T cells and APCs binding CSA1 M tumor Ags in vivo. The IL-2- and IFN-gamma-producing capacities decreased with the progress of tumor-bearing stages. This was parallel to the levels of IL-2 and IFN-gamma mRNAs expressed by cultured spleen cells. In contrast, comparable levels of TNF mRNA were expressed by all groups of cultured cells. However, large amounts of TNF were secreted by the cells from early but not from late tumor-bearing mice. TNF was produced mainly by the non-T cell fraction upon stimulation with CD4+ T cell-derived IFN-gamma. Therefore, the reduced TNF production by whole spleen cells from late tumor-bearing mice was restored by addition of rIFN-gamma to their cultures. Reciprocally to the progressive decrease in the production of IFN-gamma/TNF, the capacities of tumor-bearing mice to produce TGF-beta and IL-6 increased along with tumor growth. TGF-beta suppressed production of IL-2, IFN-gamma, and TNF, but not of IL-6. Moreover, IFN-gamma/TNF production was negatively regulated by IL-6. Taken together with the fact that the growth of CSA1 M cells is completely inhibited by the combination of TNF and IFN-gamma, these results demonstrate that the tumor-bearing state induces an abnormal cytokine network under which the production of antitumor cytokines is negatively regulated.
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PMID:Regulatory mechanisms for production of IFN-gamma and TNF by antitumor T cells or macrophages in the tumor-bearing state. 786

The gene encoding for a major surface glycoprotein, gp63, of Leishmania major was cloned into the eukaryotic expression plasmid pCDNAI with CMV or RSV promoters. The highly susceptible Balb/c mice were injected intramuscularly with 100 micrograms/mouse of the purified plasmid. The plasmids were found to be stable in vivo for at least 40 days after injection and expressed significant levels of gp63, demonstrable by immunohistological staining with specific antibody. The immunized mice developed significant resistance against L. major infection compared to controls similarly immunized with the empty plasmid. Spleen cells from the immunized mice produced significant levels of IL-2 and IFN-gamma but no detectable IL-4 when cultured with leishmanial antigens in vitro.
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PMID:Genetic vaccination against leishmaniasis. 787 20

The study by use of immunocytochemical methods shows that the spleen of mouse infected intravenously by Histoplasma capsulatum is heavily infiltrated by macrophages. The CD4+ and CD8+ T cells are diffused and sparsely distributed throughout the spleen. It appears that experimental histoplasmosis in animals presents as a disease of the mononuclear phagocyte systems. Macrophages are important cells in controlling replication of intracellular H. capsulatum. Factors that affect the infiltration and activation of macrophages are, thus, important in host defense against histoplasmosis. Depletions of endogenous TNF-alpha in animals infected with sublethal dose of H. capsulatum results in death of these animals. The fungus burden in these animals is high and macrophages are not capable of restricting proliferations of the fungus. However, the role of TNF-alpha in histoplasmosis is not a direct activation of macrophages and is still yet to be defined. IFN-gamma has been shown to fully activate mouse peritoneal macrophages and partially activate splenic macrophages for anti-histoplasma activity. The importance of IFN-gamma in host defense against histoplasmosis is studied by use of resistant A/J and susceptible C57BL/6 mouse strains. There is a good correlation of early production of IFN-gamma by spleen cells of infected mice with the ability of the animals to clear the infection. Spleen cells of resistant A/J mice are more efficient than susceptible C57BL/6 mice in production of IFN-gamma. Recombinant inbred progeny of A/J and C57BL/6 mice are used to locate the genes that control resistance to histoplasmosis. Preliminary studies show that the resistance phenotype is controlled not by a single gene but by multiple genes.
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PMID:Resistance mechanisms in murine experimental histoplasmosis. 790 6

Previous studies of mice have implicated natural killer (NK) cells as mediators of protective activity against Toxoplasma gondii through their production of gamma interferon (IFN-gamma). In the present study, we have compared NK-cell activity in infected and uninfected SCID mice. Our data reveal that infection results in increased levels of IFN-gamma in serum and elevated NK-cell activity but that these NK cells were not cytotoxic for T. gondii-infected P815 cells. Treatment with anti-IFN-gamma antibody abrogated the increase in NK-cell activity and resulted in earlier mortality of infected mice. In vivo treatment with anti-asialo GM1 antiserum reduced NK cell activity and levels of IFN-gamma in serum but did not alter time to death. Spleen cells from infected mice produced higher levels of IFN-gamma than those from uninfected mice when stimulated in vitro with live T. gondii or parasite antigen preparations. Further analysis revealed that interleukin 10 (IL-10) inhibited, whereas tumor necrosis factor alpha (TNF-alpha) and IL-12 enhanced, IFN-gamma production by spleen cells from infected or uninfected mice. The combination of IL-12 and TNF-alpha induced higher levels of IFN-gamma from whole spleen cells of infected mice than from those of uninfected mice. Depletion of the adherent cell population from the spleen cells of infected mice led to a significant reduction in the levels of IFN-gamma produced after stimulation with IL-12 plus TNF-alpha. Similar results did not occur with cells from uninfected mice. These data indicate that other cytokines produced by the adherent cell population from infected mice may be involved in maximal production of IFN-gamma by NK cells stimulated with IL-12 and TNF-alpha. To assess the importance of endogenous IL-12, a polyclonal anti-IL-12 was administered to infected SCID mice. This treatment led to earlier mortality, indicating that endogenous IL-12 mediates resistance to T. gondii.
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PMID:Production of gamma interferon by natural killer cells from Toxoplasma gondii-infected SCID mice: regulation by interleukin-10, interleukin-12, and tumor necrosis factor alpha. 791 85

Salivary gland extract (SGE) of the blood-feeding black fly Simulium vittatum is known to modulate immunological responses. In the present study, the ability of S. vittatum SGE to modulate responses during heterologous antigenic challenge was investigated in a murine model, with particular emphasis on characterizing the patterns of cytokine response. Mice were injected repeatedly with SGE or saline (sham), then challenged with the T dependent antigen ovalbumin (OVA) to generate antigen-specific lymphoblasts. Spleen cells from OVA-primed mice were then co-cultured with OVA in vitro to stimulate cytokine secretion. Cells from mice that had been injected with SGE prior to OVA challenge produced lower levels of interleukins 5 and 10 (IL-5 and IL-10) in in vitro culture, when stimulated with OVA, compared to mice that had been sham-injected with saline. Levels of IFN-gamma, IL-2 and IL-4 did not differ significantly between SGE- and saline-injected groups. Mice injected repeatedly with SGE prior to OVA challenge had fewer circulating eosinophils than sham-injected mice, while other leukocyte levels were unaffected by SGE. Prior exposure to SGE did not affect levels of serum IgE or IgA significantly. The effect of SGE on the ability of murine spleen cells to respond in vitro to the recombinant cytokines IL-2 and IL-4 was also investigated. Naive spleen cells pre-incubated with SGE proliferated less in response to both IL-2 and IL-4 in in vitro culture than cells pre-incubated with saline as a control.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Modulation of murine cellular immune responses and cytokines by salivary gland extract of the black fly Simulium vittatum. 793 61

Spleen and lymph node cells of Trypanosoma cruzi-infected mice were studied for mitogen-induced responsiveness in terms of proliferation and lymphokine production (IL-2, IFN-gamma). Splenocyte (SP) as well as lymph node cell (LN) proliferation and IL-2 production were depressed during the acute phase of the infection. Proliferative capacity of LN cells recovered completely and that of SP partially during the chronic phase. In contrast to these suppressive effects, the mitogen-induced IFN-gamma response was enhanced. In vitro co-incubation of normal SP or LN cells with trypomastigotes resulted in a reduced mitogen-induced cell proliferation and IL-2 secretion, similar to those seen with cells taken from infected mice. In contrast, trypomastigotes exerted a stimulatory activity on the mitogen-induced IFN-gamma response of both SP and LN cells. Addition of lymph node cells from T. cruzi-infected mice (LN-I) to lymph node cells of control mice (LN-C) suppressed strongly the mitogen-induced responsiveness of such cocultures. A marginal level of suppression was recorded in cocultures of spleen cells from infected mice (SP-I) and control spleen cells (SP-C). The potent suppressive cells within LN-I populations were identified as macrophage-like and such cells were absent in SP-C and peritoneal exudate cells from T. cruzi infected animals.
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PMID:Modulation of T-cell responsiveness during Trypanosoma cruzi infection: analysis in different lymphoid compartments. 801 58

We developed a convenient and reliable procedure for the cell-mediated passive transfer of type II collagen (CII)-induced arthritis (CA). Spleen cells from DBA/1 mice with CA were intravenously transferred into syngeneic recipient mice. Arthritis developed only in those recipients which had received whole-body x-irradiation (8 Gy) just before cell transfer and intraperitoneally given soluble CII without adjuvant immediately after transfer. Non-immunized splenocytes could not induce arthritis even in irradiated recipients given soluble CII. Development of arthritis depended on the number of cells transferred; 5 x 10(7) cells induced severe and long-lasting arthritis in every recipient approximately 10 days after transfer. Severity of this arthritis was clinically and histologically similar to classical CA in donors. Arthritogenic splenocytes were generated in donors no later than 20 days after priming with CII in Freund's complete adjuvant, when arthritis had yet to occur, and were detected for more than 5 weeks. One splenocyte population responsible for transferring arthritis was CD4+ T cells. We then applied this system to show that prophylactic treatment of CII-immunized mice with cyclophosphamide (CY, 7 mg/kg), but not interferon-gamma (IFN-gamma, 10(5) U/mouse), suppressed the arthritogenic ability of their spleen cells, although both treatments inhibited the development of CA. Treatment of recipients with IFN-gamma, however, inhibited the development of arthritis upon transfer with CII-immunized splenocytes. These results indicate that CY and IFN-gamma act at the induction and effector phases of arthritogenic lymphocytes, respectively. Thus, this system facilitates investigation of pathological mechanisms of CA, and of mechanisms of anti-arthritics.
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PMID:Cell-mediated transfer of collagen-induced arthritis in mice and its application to the analysis of the inhibitory effects of interferon-gamma and cyclophosphamide. 809 77

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