scholarly journals EFFECT OF NORMAL AND ACTIVATED HUMAN MACROPHAGES ON TOXOPLASMA GONDII

1974 ◽  
Vol 139 (5) ◽  
pp. 1154-1174 ◽  
Author(s):  
Seth E. Anderson ◽  
Jack S. Remington
Keyword(s):  
Toxoplasma Gondii ◽  
Cell Mediated Immunity ◽  
Blood Monocytes ◽  
Effector Cells ◽  
Human Macrophages ◽  
Obligate Intracellular ◽  
Normal Human ◽  
Induction Of Resistance ◽  
In Vitro Induction

Human macrophages derived from in vitro culture of peripheral blood monocytes were studied under a variety of conditions to determine their microbicidal capacity for the obligate intracellular protozoan, Toxoplasma gondii. The effect of macrophages on intracellular Toxoplasma was evaluated morphologically by light and phase microscopy and by autoradiography. When macrophages from dye test (DT)-negative or DT-positive individuals were infected with Toxoplasma in the presence of normal human serum, the organisms were able to multiply intracellularly with resultant destruction of the monolayer. Once organisms were intracellular, the presence of antibody-containing serum in the medium did not alter this inability of the macrophages to kill Toxoplasma. However, when Toxoplasma were incubated in the presence of heat-inactivated DT-positive serum just before infection of the monolayers, the intracellular organisms were inhibited or killed by normal macrophages. Attempts were made to activate macrophages in vitro to kill Toxoplasma. Macrophages incubated in the presence of sensitized lymphocytes and Streptokinase-Streptodornase (SK-SD) or Toxoplasma lysate antigen (TLA) were found to kill Toxoplasma when compared to macrophages incubated in the presence of lymphocytes from DT-negative individuals and TLA or lymphocytes alone. Thus, in vitro induction of resistance (both specifically and nonspecifically) in human macrophages was accomplished by culturing these cells in the presence of specifically sensitized lymphocytes and antigen. These results suggest that, as in the mouse model, activated human macrophages have the ability to inhibit or kill intracellular Toxoplasma and that these cells may be important as effector cells in cell-mediated immunity (CMI) to toxoplasmosis in man.

In vitro growth inhibition of a broad spectrum of tumor cell lines by activated human dendritic cells

Blood ◽  
2000 ◽  
Vol 95 (7) ◽  
pp. 2346-2351 ◽  
Author(s):  
Andrei I. Chapoval ◽  
Koji Tamada ◽  
Lieping Chen
Keyword(s):  
Dendritic Cells ◽  
Growth Inhibition ◽  
Wide Spectrum ◽  
Human Tumor ◽  
Interferon Γ ◽  
Interleukin 4 ◽  
Tumor Resistance ◽  
Blood Monocytes ◽  
Effector Cells

Dendritic cells (DCs) are critical subsets of leukocytes providing antigen presentation for initiation of humoral and cellular immune responses. Their role as effector cells in tumor resistance, however, is less known. We report here that human DCs generated by culturing plastic-adherent peripheral blood monocytes in the presence of granulocyte-monocyte colony–stimulating factor (GM-CSF) and interleukin-4 have potent growth-inhibition activity in vitro on a wide spectrum of human tumor lines of different tissue origin. Proinflammatory stimuli lipopolysaccharide (LPS) and interferon-γ, but not tumor necrosis factor– and CD40 signaling, can further enhance DC-mediated inhibition of tumor growth. The growth inhibition requires contact between DCs and tumor cells while LPS treatment enhances the antitumor activity in DC culture supernatants. Our results suggest that in addition to their predominant role as regulatory cells, activated DCs are also potential effector cells in tumor immunity.

scholarly journals Infection of primary human macrophages with hepatitis C virus in vitro: induction of tumour necrosis factor-α and interleukin 8

2004 ◽  
Vol 85 (1) ◽  
pp. 47-59 ◽  
Author(s):  
Marek Radkowski ◽  
Agnieszka Bednarska ◽  
Andrzej Horban ◽  
Janusz Stanczak ◽  
Jeffrey Wilkinson ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Tumour Necrosis Factor Α ◽  
Human Macrophages ◽  
Factor Α ◽  
In Vitro Induction ◽  
Necrosis Factor

In vitro induction of resistance to metronidazole, and analysis of mutations in rdxA and frxA genes from Helicobacter pylori isolates

2005 ◽  
Vol 11 (2) ◽  
pp. 59-63 ◽  
Author(s):  
Luis Perez Aldana ◽  
Takeshi Kondo ◽  
Rinan Zheng ◽  
Toshio Sugiyama ◽  
Masahiro Asaka ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Induction Of Resistance ◽  
In Vitro Induction

scholarly journals Rosette-forming ability of thymus-derived lymphocytes in cell-mediated immunity. I. Delayed hypersensitivity and in vitro cytotoxicity.

1975 ◽  
Vol 141 (3) ◽  
pp. 584-599 ◽  
Author(s):  
B E Elliott ◽  
J S Haskill ◽  
M A Axelrad
Keyword(s):  
T Cell ◽  
In Vitro Cytotoxicity ◽  
Delayed Hypersensitivity ◽  
Velocity Sedimentation ◽  
Target Cells ◽  
Cell Mediated Immunity ◽  
Small Lymphocyte ◽  
Effector Cells ◽  
Effector T Cell

Effector cells in delayed hypersensitivity and in vitro cytotoxicity were studied in lymph node cells from animals immunized with sheep erythrocytes (SRBC) in complete Freund's adjuvant. Delayed hypersensitivity response (DHR) was assayed by the increase in foot pad swelling after the intrafoot pad injection of immune cells plus antigen. Cell-mediated cytotoxicity against SRBC was assayed by a microcytotoxicity test with sheep fibroblasts as target cells. Effector cells were antigen specific, sensitive to anti-theta serum plus complement (C), and insensitive to anti-Ig serum plus C. A nonrosette-forming (non-RFC) small lymphocyte effector T cell and a rosette-forming medium lymphocyte effector T cell were isolated by velocity sedimentation. The small lymphocyte non-RFC required a longer time than the medium lymphocyte RFC effector cell to produce maximum activity. Buoyant density failed to distinguish medium lymphocyte effector cells in DHR and in vitro cytotoxicity.

scholarly journals A Rapid Flow Cytometric Method to Explore Cellular Immunity against Toxoplasma gondii in Humans

1998 ◽  
Vol 5 (6) ◽  
pp. 745-748 ◽  
Author(s):  
Sandrine Kahi ◽  
Grégoire J. N. Cozon ◽  
Timothy Greenland ◽  
Martine Wallon ◽  
Françoise Gay-Andrieu ◽  
...  
Keyword(s):  
T Cells ◽  
Toxoplasma Gondii ◽  
T Lymphocytes ◽  
Congenital Infection ◽  
Cell Mediated Immunity ◽  
Flow Cytometric Method ◽  
Flow Cytometric ◽  
Excellent Candidate ◽  
Activation Antigens

ABSTRACT To assess cell-mediated immunity to Toxoplasma gondii, we evaluated the expression of the activation antigens CD69, CD71, and CD25 on T lymphocytes by flow cytometry after specific in vitro stimulation of whole blood from 127 T. gondii-positive and 63 T. gondii-negative patients. T lymphocytes from many seropositive individuals did not express CD69 at 24 h afterT. gondii antigen stimulation, but CD71 and CD25 were easily detectable on T cells from seropositive individuals 7 days after specific activation. CD25 was mainly expressed by stimulated CD4+ T cells, and its detection on total T cells was both a sensitive (98%) and a specific (97%) indicator of prior T. gondii infection. These results make flow cytometric detection of CD25 an excellent candidate for screening cell-mediated immunity toT. gondii in vitro and an interesting tool for the diagnosis of congenital infection.

In vitro recovery of insulin binding after downregulation in cultured normal human monocytes

1985 ◽  
Vol 249 (1) ◽  
pp. E94-E98
Author(s):  
R. H. Whitson ◽  
S. A. Kaplan
Keyword(s):  
Human Peripheral Blood ◽  
Insulin Receptors ◽  
Insulin Binding ◽  
Blood Monocytes ◽  
Peripheral Blood Monocytes ◽  
Surface Receptors ◽  
Normal Human ◽  
Lysosomal Proteases ◽  
Normal Human Peripheral Blood

When normal human peripheral blood monocytes were treated with insulin in vitro, surface insulin receptors disappeared rapidly, but total insulin receptors (surface and internalized receptors), measured in detergent-solubilized extracts of total cellular membranes, decreased slowly. Surface receptors decreased to 51 +/- 4, 36 +/- 12, and 34 +/- 12%, of control levels after 2, 6, and 18 h of insulin pretreatment, respectively. Total receptors decreased to 86 +/- 12, 69 +/- 17, and 34 +/- 12% of control levels in the same periods. Chloroquine, a lysosomotropic agent, inhibited the removal of surface receptors, indicating that lysosomal proteases play a role in this process. Unlike monocytes, IM-9 lymphocytes lost surface receptors and total receptors at the same rate when incubated with insulin. Monocytes treated with insulin for 18 h, washed free of unbound insulin and recultured for 48 h regained 94 +/- 7% of control insulin binding, indicating that cultured monocytes are competent to regenerate their insulin receptors. Monocytes treated with insulin for 6 h also required 48 h to recover their insulin binding, despite the fact that substantial numbers of insulin receptors remained intact within these cells. Two-hour pretreated monocytes recovered somewhat faster, attaining control levels of receptors after 24 h of reculture. This suggests that internalized insulin receptors pass from a recyclable pool to a nonrecyclable one.

Macrophage function and host resistance against infection with Toxoplasma gondii

1976 ◽  
Vol 22 (10) ◽  
pp. 1453-1457 ◽  
Author(s):  
H. Hof ◽  
K. Höhne ◽  
H. P. R. Seeliger
Keyword(s):  
Toxoplasma Gondii ◽  
Dextran Sulfate ◽  
Effector Cells ◽  
Macrophage Function ◽  
Obligate Intracellular ◽  
Carbon Particles ◽  
Increased Susceptibility ◽  
Stimulation Of

The role of macrophages on the course of an infection with Toxoplasma gondii has been examined. Stimulation of macrophage function by killed Bordetella pertussis cells did not show any beneficial effect as an increased susceptibility became apparent. The functional blockade of macrophages by dextran sulfate or carbon particles did not result in a higher susceptibility of mice to the lethal primary infection with T. gondii. Thus in vivo macrophages apparently do not play an essential role as effector cells as they do in infections with other obligate intracellular infective organisms such as Listeria monocytogenes.The spleen is apparently of crucial importance for resistance against T. gondii infection, since death occured earlier in splenectomized mice than in control animals.

Human Macrophages Phagocytose Rituximab Opsonised Leukemic Cells Via CD16, CD32 and CD64 but Do Not Mediate ADCC.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 2507-2507
Author(s):  
Josee Golay ◽  
Marzia Leidi ◽  
Giuseppe A. Palumbo ◽  
Martino Introna
Keyword(s):  
Complement Activation ◽  
Xenograft Model ◽  
Lymphocytic Leukemia ◽  
Leukemic Cells ◽  
Therapeutic Activity ◽  
Blood Monocytes ◽  
Response Curves ◽  
Human Macrophages

Abstract Rituximab (Mabthera®) is a chimeric monoclonal IgG1 antibody with therapeutic activity in non-Hodgkin B lymphomas (B-NHL) and B-Chronic Lymphocytic Leukemia (B-CLL). We have recently obtained evidence, using a bulky lymphoma xenograft model in nude mice, that both complement and macrophages are required for the therapeutic activity of rituximab. In order to further investigate the tumor cell killing potential of macrophages and its modulation by different factors, including complement, we have set up in vitro experiments with purified macrophage populations. Human macrophages were obtained from purified peripheral blood monocytes cultured for 4 days in presence of 20% FCS and 20 ng/ml M-CSF. FACS analysis confirmed the phenotype of these cells including CD11b and FcγRs expression (CD16, CD32, CD64). Phagocytosis assays were then carried out with CLL cell as targets in presence or absence of increasing concentrations of rituximab. Phagocytosis was evaluated by counting under an inverted microscope the stained cytospin preparations. From 9.8% to 60.8% of macrophages engulfed at least one tumor target cell in a series of 24 experiments (mean 29.7%± 18.3%). Control irrelevant IgG1k monoclonal antibodies (anti-erbB2 trastuzumab and anti-EGFR cetuximab) did not mediate phagocytosis, and rituximab did not lead to ingestion of CD20 negative cells, demonstrating the specificity of the assay. Phagocytosis was already maximal at around 0.1 μg/ml rituximab concentration. In contrast complement activation required Mab concentration of at least 1 μg/ml. Thus phagocytosis, like ADCC, is active at about 10 fold lower MAb concentrations than complement triggering. Levels of CD20 expression on targets did not significantly affect phagocytosis. The role of different FcγRs was also investigated by addition 5 μg/ml blocking antibodies to CD16, CD32 and CD64. All 3 blocking Mabs reduced significantly phagocytosis (by 45%, 42% and 40% respectively with respect to control). Inhibition increased to 64% in presence of all 3 antibodies. Since previous data had suggested a role of the Val/Phe polymorphism at position 158 of CD16A in the clinical response of lymphoma patients to rituximab as well as in NK-mediated ADCC, we investigated whether this polymorphism also affected phagocytosis. No significant differences in dose response curves were observed using macrophages from either Val-Val or Phe-Phe homozygotes. Perhaps surprisingly, concomitant complement activation induced by addition of human serum did not increase phagocytosis. Whether human macrophages can also mediate antibody dependent cellular cytotoxicity (ADCC) was also studied. CLL or BJAB cells were labeled with Calcein-AM and ADCC measured as released fluorescence after 4 hours at 37°C. Macrophages were unable to mediate ADCC in presence of rituximab even following treatment with IFNγ (100 U/ml) for 48 hours. We conclude that macrophages efficiently mediate phagocytosis but not ADCC in presence of low concentrations of rituximab.

Sign in / Sign up

Export Citation Format

Share Document