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V Brinkmann

Publications and source records attributed to V Brinkmann.

64 records · Page 4Linked to original sources
PubMed1986

Different regulation of the L3T4-T cell subset by B cells in different mouse strains bearing the H-2k haplotype.

Splenic L3T4-T cells from Toxoplasma gondii-infected CBA/J (H-2k, Igh 1a) but not C3H/He (H-2k, Igh 1j) mice responded with marked antigen-specific proliferation and interleukin 2 (IL 2) production, as well as concanavalin A-induced proliferation. The proliferative response of C3H/He spleen cells could be restored in part in vitro by addition of exogenous recombinant IL 2. The observed unresponsiveness of C3H/He spleen cells was due to the release of IL 2-inhibiting factors. These factors, present in culture supernatants from antigen restimulated C3H/He spleen cells, blocked the growth of an IL 2-dependent T cell line in the presence of optimal concentration of IL 2. During the early stages of infection, C3H/He splenic macrophages lacked the capacity to present antigen. In addition a nonspecific B cell-mediated suppression of T cell proliferation was observed. In later stages of infection macrophages displayed normal antigen-presenting function in comparison with macrophages of normal uninfected mice. At this stage of infection nonspecific, minor histocompatibility restricted B cell suppression was observed. These results suggest a possible role of B cells in regulation of T cell immunity to T. gondii.

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PubMed1986

Autoreactive T cell clones from mice infected with Mycobacterium bovis, strain Bacillus Calmette-Guérin (BCG). I. Phenotype, specificity and in vitro function.

Mice were infected with the intracellular microorganism, Mycobacterium bovis BCG, and draining lymph node cells were collected. A T cell line was established which was cultured in the presence of syngeneic accessory cells (AC) and killed BCG. Stimulation of this line depended on syngeneic accessory cells and did not require BCG as a source of antigen, indicating that it was autoreactive. T cell clones derived from this line had the L3T4 helper/inducer phenotype and reacted with self-Ia on syngeneic macrophages or B cell blasts. Cloned T cells were also stimulated by syngeneic accessory cells pretreated with the lysosomotropic agent chloroquine and by H-2 compatible, background gene disparate, accessory cells, suggesting that they were specific for self-Ia. After in vitro stimulation, the T cell clones secreted interleukin 2 (IL 2) and interferon-gamma (IFN-gamma), helped B cells in antibody production and activated macrophages for secretion of reactive oxygen metabolites.

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PubMed1985

T-cell-mediated immune response in murine malaria: differential effects of antigen-specific Lyt T-cell subsets in recovery from Plasmodium yoelii infection in normal and T-cell-deficient mice.

For analysis of the role of immune T cells in protective immunity against murine malaria, Plasmodium yoelii-immune Lyt T-cell subsets were functionally characterized in vitro and in vivo. Selected Lyt2- and Lyt2+ T cells from P. yoelii-immune C57BL/10 mice differed in their capability to proliferate in response to P. yoelii antigen in vitro. Only the Lyt2- T-cell population produced T-cell growth factor upon restimulation, and none of the selected T-cell subsets produced detectable amounts of macrophage activating factor. Lyt2- but not Lyt2+ lymphocytes were capable of transferring protection to normal C57BL/10 mice. When transferred into T-cell-deficient C57BL/6-nu/nu mice, adoptive resistance to P. yoelii by Lyt2- lymphocytes was only demonstrable after prior reconstitution of recipients with normal T cells. These results suggest an interaction between P. yoelii-immune Lyt2- T cells and normal T lymphocytes via T-cell growth factor in the development of protective immunity to malaria.

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PubMed1984

Attempts to characterize the T-cell population and lymphokine involved in the activation of macrophage oxygen metabolism in murine listeriosis.

Cultures of T cells from Listeria monocytogenes-immune mice, macrophages, and heat-killed Listeria organisms produced a factor(s) capable of activating macrophage oxygen metabolism. The activity depended on the presence of Lyt 1+2,3- T cells in the primary culture. Macrophage oxygen metabolism could also be induced by a L. monocytogenes-specific T-cell clone which was recently shown to mediate anti-listerial protection in vivo and to secrete interferon-gamma (IFN-gamma) in vitro. Furthermore, macrophage activation was achieved by recombinant IFN-gamma. It is concluded that acquired resistance to facultative intracellular pathogens--at least in part--depends on the activation of macrophage oxygen metabolism by IFN-gamma derived from specific Lyt 1+2,3- T cells.

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PubMed1984

Role of macrophages in malaria: O2 metabolite production and phagocytosis by splenic macrophages during lethal Plasmodium berghei and self-limiting Plasmodium yoelii infection in mice.

The role of splenic macrophages in resistance to lethal Plasmodium berghei or self-limiting Plasmodium yoelii was studied by testing their rate of phagocytosis and their production of O2 metabolites (H2O2 and O2-) upon nonspecific stimulation with zymosan. It was found that, compared with P. berghei, infection of mice with P. yoelii resulted in an earlier appearance and in higher numbers of adherent cells in the spleen. Furthermore, the capacity of macrophages to generate O2 metabolites was significantly higher in P. yoelii- than in P. berghei-infected mice. This difference in the production of O2 metabolites was more pronounced when calculated on a per spleen basis. On the other hand, phagocytosis by macrophages was similar in both types of infection. The data suggest that lethal and nonlethal malaria species differ in their capacity to induce the production of O2 metabolites by macrophages, thereby influencing the final course of disease.

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PubMed1982

Chemiluminescence response of peritoneal macrophages to parasitized erythrocytes and lysed erythrocytes from Plasmodium berghei-infected mice.

The chemiluminescence response of normal mouse peritoneal macrophages to parasitized erythrocytes isolated from mice 3 weeks after infection with Plasmodium berghei was examined. Only 4 of 12 animals showed positive responses, whereas 8 showed negative responses. Photomicrographs revealed that only in chemiluminescence-positive animals were parasitized erythrocytes attached to or phagocytized by macrophages. When lysed parasitized-erythrocyte cell suspensions were added to the peritoneal macrophages, chemiluminescence could be induced in all cases. The response was enhanced remarkably by the addition of very small amounts of immune serum. Normal macrophages activated in vitro by supernatant from antigen-stimulated spleen cells from immune mice showed much higher parasite-induced chemiluminescence responses than did nonactivated macrophages, especially in the presence of immune serum.

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PubMedDate not supplied

Control of intestinal allograft rejection by FTY720 and costimulation blockade.

INTRODUCTION: The clinical application of small bowel transplantation (SBTx) is hampered by its pronounced immunogenicity. In this study we examined the effects of the novel immunosuppressant FTY720 and costimulation blockade by an anti-CD40L mAb (MR-1) in a stringent mouse model of SBTx. METHODS: SBTx was performed in mice with a full MHC mismatch (donors: C3H=H-2(k); recipients: C57BL/6=H-2(b)). Recipients were divided into four groups: 1, untreated group; 2, MR1 monotherapy (500 microg IV on days 0, 2, 4, and 7); 3, FTY720 monotherapy (1 mg/kg body weight PO for 14 consecutive days after transplantation); 4, FTY720 plus MR1-treated group. Graft rejection grades were assessed by H&E staining. Graft mesenteric lymph nodes (MLNs), Peyer's patches (PPs), as well as intraepithelial lymphocytes (IELs) and lamina propria lymphocytes (LPLs) were analyzed by flow cytometry and three-color immunofluorescence staining. RESULTS: Neither FTY720 nor MR1 monotherapy was efficient in preventing the rejection of mouse intestinal allografts, whereas FTY720 plus MR1 profoundly inhibited the rejection response at the 14th posttransplant day. The infiltration of host lymphocytes was reduced in graft MLNs, PPs, IELs, and LPLs by FTY720 therapy. FTY720 plus MR1 inhibited host CD8(+) T-cell infiltration in graft LPLs when compared with grafts treated with FTY720 only. Additionally, two subpopulations, CD11b(+high) Gr1(-) and CD11b(+intermediate) Gr1(+) cells, were decreased in FTY720-treated grafts. CONCLUSIONS: FTY720 plus MR1 efficiently delayed intestinal allograft rejection in a mouse model by preventing the infiltration of host lymphocytes, particularly of CD8(+) cells.

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