scholarly journals Increased Capacity for Interleukin-2 Synthesis Parallels Disease Progression in Mice Infected withLeishmania major

1998 ◽  
Vol 66 (9) ◽  
pp. 4537-4540 ◽  
Author(s):  
Frederick P. Heinzel ◽  
Ronald M. Rerko ◽  
Andrea M. Hujer ◽  
Richard A. Maier
Keyword(s):  
Lymph Node ◽  
Disease Progression ◽  
Functional Significance ◽  
Interleukin 2 ◽  
Gamma Interferon ◽  
Mrna Levels ◽  
Lymph Node Cells

ABSTRACT Lymph node cells of BALB/c mice with progressive leishmaniasis produced sixfold more interleukin-2 (IL-2) in culture than those of healing C57BL/6 mice. IL-2 synthesis also increased in C57BL/6 mice made susceptible by IL-12 or gamma interferon deficiency. However, IL-2 mRNA levels in vivo did not reflect IL-2 production in vitro. Because IL-2 contributes to the pathogenesis of progressive leishmaniasis, the functional significance of these findings should be further explored.

In vitro lymphocyte recognition of islet cells following in vivo priming with allogeneic murine pancreatic islets

1984 ◽  
Vol 105 (1) ◽  
pp. 87-92 ◽  
Author(s):  
Joanne Scott ◽  
Peter G. MacKay ◽  
Åke Lernmark
Keyword(s):  
Lymph Node ◽  
Pancreatic Islets ◽  
Islet Cell ◽  
Islet Cells ◽  
Culture Conditions ◽  
Pancreatic Tissue ◽  
Insulin Dependent ◽  
Lymph Node Cells

Abstract. Lymphocytes from patients with insulin-dependent diabetes have been shown to be sensitized to pancreatic tissue antigens. Mice immunized with homologous pancreatic islets have been found to develop glucose intolerance and insulitis. Since lymphocytes may be involved in diabetogenesis, we wished to determine if lymph node cells from islet-immunized mice can recognize and respond to islet cells in vitro. A.TL female mice were immunized with an emulsion of BALB/c islet homogenate and complete Freund's adjuvant (CFA); sham-treated A.TL mice were injected with adjuvant and water. Mice were sacrificed 7–8 days later and the draining lymph nodes were removed. The lymph node cells were co-cultured with freshly prepared irradiated BALB/c islet cell, which served as stimulator cells. The co-cultures were incubated for 24–26 h at 37°C, followed by a 16 h [3H]thymidine (TdR) pulse. A significant proliferation of lymph node cells from islet-primed mice was induced during the in vitro stimulation with irradiated islet cells when compared with lymph node cells from sham-treated mice (P < 0.001). The response may be islet-cell-specific, since irradiated lymph node cells from BALB/c mice failed to proliferative response under the same culture conditions (P > 0.80).

scholarly journals Recombinant Galectin-1 and Its Genetic Delivery Suppress Collagen-Induced Arthritis via T Cell Apoptosis

1999 ◽  
Vol 190 (3) ◽  
pp. 385-398 ◽  
Author(s):  
Gabriel A. Rabinovich ◽  
Gordon Daly ◽  
Hanna Dreja ◽  
Hitakshi Tailor ◽  
Clelia M. Riera ◽  
...  
Keyword(s):  
Lymph Node ◽  
T Cell ◽  
Interleukin 2 ◽  
Disease Onset ◽  
Therapeutic Effects ◽  
Collagen Induced Arthritis ◽  
Gene Therapy Protocol ◽  
Lymph Node Cells

Galectin-1 (GAL-1), a member of a family of conserved β-galactoside–binding proteins, has been shown to induce in vitro apoptosis of activated T cells and immature thymocytes. We assessed the therapeutic effects and mechanisms of action of delivery of GAL-1 in a collagen-induced arthritis model. A single injection of syngeneic DBA/1 fibroblasts engineered to secrete GAL-1 at the day of disease onset was able to abrogate clinical and histopathological manifestations of arthritis. This effect was reproduced by daily administration of recombinant GAL-1. GAL-1 treatment resulted in reduction in anticollagen immunoglobulin (Ig)G levels. The cytokine profile in draining lymph node cells and the anticollagen IgG isotypes in mice sera at the end of the treatment clearly showed inhibition of the proinflammatory response and skewing towards a type 2–polarized immune reaction. Lymph node cells from mice engaged in the gene therapy protocol increased their susceptibility to antigen-induced apoptosis. Moreover, GAL-1–expressing fibroblasts and recombinant GAL-1 revealed a specific dose-dependent inhibitory effect in vitro in antigen-dependent interleukin 2 production to an Aq-restricted, collagen type 2–specific T cell hybridoma clone. Thus, a correlation between the apoptotic properties of GAL-1 in vitro and its immunomodulatory properties in vivo supports its therapeutic potential in the treatment of T helper cell type 1–mediated autoimmune disorders.

scholarly journals A STUDY OF THE DISTRIBUTION OF 2,4-DINITROBENZENE SENSITIZERS BETWEEN ISOLATED LYMPH NODE CELLS AND EXTRACELLULAR MEDIUM IN RELATION TO INDUCTION OF CONTACT SKIN SENSITIVITY

1959 ◽  
Vol 110 (2) ◽  
pp. 187-206 ◽  
Author(s):  
Herman N. Eisen ◽  
Milton Kern ◽  
William T. Newton ◽  
Ernst Helmreich
Keyword(s):  
Molecular Weight ◽  
Lymph Node ◽  
Low Molecular Weight ◽  
Skin Sensitivity ◽  
Extracellular Medium ◽  
Protein Conjugates ◽  
Protein Conjugate ◽  
Lymph Node Cells

Although induction of contact skin sensitivity by low molecular weight 2,4-dinitrobenzenes requires the formation in vivo of 2,4-dinitrophenyl-proteins, analogous protein conjugates prepared in vitro are unable to induce this hypersensitive state. Low molecular weight 2,4-dinitrobenzenes are concentrated by isolated lymph node cells, but a representative 2,4-dinitrophenyl-protein conjugate (2,4-dinitrophenyl-bovine serum albumin) was not taken up to a detectable extent by these cells. It is inferred that there exist large quantitative differences in the extent to which dinitrophenyl-proteins are localized within cells following the administration to an intact animal of (a) those simple dinitrobenzenes which are both concentrated by lymph node cells and have the capacity to form protein conjugates in vivo, and (b) 2,4-dinitrophenyl-protein conjugates prepared in vitro. It is suggested that this difference could account for the fact that a varietyof 2,4-dinitrophenyl-proteins prepared in vitro are unable to induce contact skin sensitivity.

scholarly journals Mechanisms of Immunosuppression: Effects of Cyclophosphamide on Cellular Immunity

Blood ◽  
1973 ◽  
Vol 41 (2) ◽  
pp. 273-284 ◽  
Author(s):  
Alan Winkelstein
Keyword(s):  
Lymph Node ◽  
Cellular Immunity ◽  
Substantial Reduction ◽  
Lymphoid Cells ◽  
In Vitro Tests ◽  
Migration Inhibition ◽  
Cutaneous Hypersensitivity ◽  
Lymph Node Cells

Abstract A course of cyclophosphamide administered to guinea pigs after immunization with mycobacteria led to a transient inhibition of cutaneous hypersensitivity to tuberculin protein. This treatment resulted in generalized depletion of lymphoid cells, including lymphopenia, and a substantial reduction in the number of macrophages found in induced peritoneal exudates. Results of in vivo cell transfer studies indicated that cyclophosphamide-treated recipients were rendered transiently unresponsive to purified tuberculin protein (PPD). However, sensitized lymph node cells from drug-treated donors were capable of transferring immunity to normal recipients. In vitro tests of cellular immunity with lymph node cells from drug-treated animals yielded discordant results. The proliferative response to both PHA and PPD was significantly impaired. However, these lymphoid cells functioned normally in assays for migration inhibition factor (MIF). Thus, these data suggest that cyclophosphamide can limit proliferation without impairing intermitotic functions of sensitized lymphocytes, such as the release of MIF. Results of this study suggest that cyclophosphamide does not impair development of a population of specifically sensitized T-type lymphocytes. However, several components of the expression phase are affected; the resultant anergy is probably due to a summation of effects on lymphocytes and macrophages.

scholarly journals ANTAGONISTIC EFFECTS OF HUMORAL ISOANTIBODIES ON THE IN VITRO CYTOTOXICITY OF IMMUNE LYMPHOID CELLS

1965 ◽  
Vol 122 (1) ◽  
pp. 11-23 ◽  
Author(s):  
Erna Möller
Keyword(s):  
Lymph Node ◽  
Regional Lymph Node ◽  
In Vitro Cytotoxicity ◽  
Normal Serum ◽  
Lymphoid Cells ◽  
Spleen Cells ◽  
Humoral Antibodies ◽  
Lymph Node Cells

The ability of specifically immunized lymphoid cells to kill H-2 incompatible target tumor cells in tissue culture was shown to depend on the source of the lymphoid tissue (spleen versus lymph nodes). Marked cytotoxic effects were obtained with regional lymph node cells 7 to 10 days after primary immunization, whereas spleen cells from the same animals had little or no effect. Hyperimmunization did not decrease the cytotoxic efficiency of lymph node cells. Experiments were performed to test the possibility that the weak effect of spleen cells is a result of humoral antibody production, antagonizing the cell-bound immunity. Humoral antibodies were cytotoxic in vitro in the presence of complement only. Their effect was manifested after 2 hours, whereas immune lymph node cells did not require complement and cytotoxicity was not expressed until 24 to 48 hours' incubation. Tumor cell cultures treated with specific humoral antibodies in the absence of complement became resistant to the cytotoxic effect of subsequently added immune lymph node cells, while no such protection was seen when normal serum was added. Thus, humoral antibodies led to an "efferent" inhibition of cell-bound immunity in vitro, in analogy with previous results in vivo.

scholarly journals Alterations in Frequency of Interleukin-2 (IL-2)-, Gamma Interferon-, or IL-4-Secreting Splenocytes Induced by Candida albicans Mannan and/or Monophosphoryl Lipid A

1998 ◽  
Vol 66 (4) ◽  
pp. 1392-1399 ◽  
Author(s):  
Shaokang P. Li ◽  
Sang-il Lee ◽  
Judith E. Domer
Keyword(s):  
Candida Albicans ◽  
Lipid A ◽  
Interleukin 2 ◽  
Gamma Interferon ◽  
Saline Control ◽  
Immunomodulatory Activity ◽  
Monophosphoryl Lipid A ◽  
Monophosphoryl Lipid

ABSTRACT We have shown previously that intravenous injection ofCandida albicans mannan (MAN) into naive mice induced CD8+ effector downregulatory cells and that such cells were not produced if mice were deficient in CD4+ or I-A+ cells during the early interval (≤30 h) following the introduction of MAN. Moreover, the nonspecific biological response modifier monophosphoryl lipid A (MPL), given in vivo or incubated with cells in vitro, can abrogate the MAN-specific immunomodulatory activity. The mechanism by which the abrogation is mediated is unknown, but it is hypothesized to involve cytokines. Therefore, we measured the number of cytokine-secreting cells for the Th1 cytokine interleukin-2 (IL-2) and the Th2 cytokine IL-4, as well as for gamma interferon (IFN-γ), in splenocyte populations from MAN and/or MPL-treated mice, using an enzyme-linked immunospot assay designed to detect individual cytokine-secreting cells (spot-forming cells [SFC]). Cytokine-secreting cells were demonstrated in cell suspensions enriched for CD4+ cells, but no SFC could be demonstrated in populations enriched for CD8+ cells. Both MAN and MPL, when administered to separate groups of animals, stimulated the production of increased numbers of cytokine-producing cells for each of the three cytokines tested. The response with respect to IL-4-secreting cells, however, was the most striking. Despite the fact that MAN and MPL independently caused increases in SFC to all three cytokines, when both MAN and MPL were administered to the same animal, all increases were reversed, and the numbers of SFC detected were at or below those detected in saline control animals. These data support the hypothesis that IL-4 is involved in MAN-specific immunoregulatory activities. The data also emphasize the fact that two immunomodulators, i.e., MAN and MPL, having similar effects when given in vivo independently, may be antagonistic when administered sequentially to the same animal.

In vitro Synthesis of Auto-Antibodies by Rabbit Lymph Node Cells following Cross-Immunization in vivo

Nature ◽  
1962 ◽  
Vol 194 (4831) ◽  
pp. 881-882 ◽  
Author(s):  
ALAIN BUSSARD ◽  
CLAUDE HANNOUN
Keyword(s):  
Lymph Node ◽  
In Vitro Synthesis ◽  
Lymph Node Cells
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