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M Giese

Publications and source records attributed to M Giese.

5 recordsLinked to original sources
PubMed1989

Role of interleukin 1 in mycoplasma mitogen-induced proliferation of human T cells.

Recently, a mitogenic effect of the supernatant of cultured mycoplasma arthritidis (MAS) on human and murine lymphocytes has been described. Here, we studied the role of accessory cells (AC) in MAS-induced T cell proliferation in a system of human leukocytes. Nylon-wool purified T cells were non-responsive to MAS with regard to both proliferation and IFN-gamma production. The capacity of T lymphocytes to respond to MAS could be restored when viable AC were added. Treatment of AC with UV light resulted in a cell population which was incapable of reconstituting T cells. Addition of human recombinant interleukin 1 alpha (IL 1 alpha) or IL 1 beta again showed a reconstituting effect. However, only a partial reconstitution of the T cell response could be achieved by addition of recombinant IL 1 alpha or IL 1 beta. The optimal restoration was achieved by adding IL 1 at a concentration of 100 U/ml IL 1 alpha or 100 U/ml IL 1 beta. The results indicate that metabolically active AC were required for MAS-induced T cell proliferation to occur and that IL 1 was able to substitute for the role of AC. Since this restoration was only partial, it remains to be determined whether factors others than IL 1 are required to fully substitute the role of accessory cells.

Antigen-Presenting Cells↗
PubMed1988

Blocking of interferon synthesis in murine macrophages by pretreatment with interferon.

The influence of pretreatment with interferon (IFN) on subsequent IFN synthesis was investigated in macrophage cultures of DBA/2 and C57BL/6 mice. The doses of IFN alpha/beta for pretreatment ranged from 10,000 U/ml to 100 U/ml and the incubation time was between 18 and 2 h. No blocking effect was observed for chemical induction with poly I:poly C or CMA. However, for viral infection with NDV, blocking was observed. This inhibition of IFN synthesis was dependent on the dose and time of IFN pretreatment and of the titer of the inducing virus. Similarly in mouse fibroblast cultures no blocking activity was observed for induction with poly I:poly C/DEAE-dextran. Again, with NDV as inducer, pretreatment with IFN resulted in inhibition of interferon synthesis. Thus, our data show that blocking occurs only with a viral inducer and suggest that it is caused by an antiviral effect.

Animals↗
PubMed1988

[Interferons and their effects].

The interferon system is an integral part of the defense system of the body, mediating a large variety of biologic effects. Presently, three groups of interferons (IFN) are known: IFN alpha, IFN beta and IFN gamma. IFN alpha and IFN beta show homology on the nucleotide level of about 40-50%, and both IFNs bind to a common receptor. IFN alpha and IFN beta are produced after induction by leukocytes and fibroblasts. IFN gamma is, by definition, not only an interferon but also a lymphokine, since it is a product exclusively of lymphocytes. There is no homology on the nucleotide level between IFN gamma and IFN alpha/beta. Furthermore, the receptor of IFN gamma is different from the receptor of IFN alpha/beta. IFNs are defined by their antiviral activity directed against a large number of different viruses. The target of IFN is the cell rather than the virus itself. Through binding on the cell surface and subsequent activation of specific genes IFNs induce an antiviral state which makes cells less permissive for virus replication. The antiviral state consists of various antiviral mechanisms. Among the non-antiviral effects of IFNs are the effects on cellular components of the immune system. Thus, one has postulated a role for interferons as immunoregulatory molecules. Interferons augment the expression of MHC-genes of which IFN alpha/beta only affect the molecules of class I, whereas IFN gamma affects both the molecules of class I and class II. Moreover, all IFNs increase the activity of macrophages and NK cells. Possibly the activation of components of the immune system is in part responsible for the antitumor effects of interferon.(ABSTRACT TRUNCATED AT 250 WORDS)

Humans↗
PubMed1988

Contamination of a monoclonal antibody with LDH-virus causes interferon induction.

Interferon induction occurred unexpectedly during an in vivo study using a mouse monoclonal antibody. The interferon was typed alpha/beta and the titer reached a maximum at 24 hours in contrast with other inducers. Similar results were obtained with a virus pool derived from the antibody and with a LDV reference strain. MAP-testing of the monoclonal antibody revealed contamination with lactate dehydrogenase virus (LDV). The production of IFN seems to be controlled genetically. This experimental error demonstrates the importance of an appropriate quality control of biological materials.

Animals↗