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Biomedical subjects

W Fierz

Publications and source records attributed to W Fierz.

At least 55 records · Page 3Linked to original sources
PubMed1988

Immunodeficiency after major trauma and selective surgery.

The posttrauma immunodeficiency syndrome and the related postsurgery immunodeficiency syndrome are essential for the infections often occurring after polytrauma and major surgery. Data are given here showing that after such events the levels of immunoglobulins; the complement factors C3C, C4 and C Factor B; and the numbers of circulating lymphocytes and of the subpopulations CD3, CD4, CD8 and natural killer cells as well as the stimulatory capacity of mononuclear cells to mitogen fall; while the levels of acute phase proteins, neopterin and interleukin 2 receptors and the spontaneous uptake of thymidine by mononuclear cells become augmented. Extent and duration of these changes and the rate of subsequent infections depend on the extent and kind of surgery (minor, major, clean, contaminated). However, crucial factors of the posttrauma and postsurgery immunodeficiency syndromes are not yet elucidated and relevant predictive parameters for infections are not at hand. These are essential prerequisites to initiate future immunomodulatory measures which should be added to the use of intravenous immunoglobulins yielding so far distinct but limited benefits for the prevention of infections after polytrauma and major surgery.

Complement C3↗
PubMed1987

Ciclosporin A prevents P2 T cell line-mediated experimental autoimmune neuritis (AT-EAN) in rat.

Adoptive transfer experimental autoimmune neuritis (AT-EAN) produced in Lewis rats by injection of P2-reactive T lymphocyte line cells offers the unique possibility to study the exclusive contribution of cell-mediated immune responses to the pathogenesis of autoimmune disease of the peripheral nervous system (PNS). It further lends itself to the evaluation of novel therapeutic approaches that may bear relevance to the human acute Guillain-Barré syndrome. The effects of the immunosuppressive agent ciclosporin A on the clinical, electrophysiological and morphological expression of AT-EAN were examined. We found that ciclosporin A suppressed development of the disease. In view of the known actions of ciclosporin A on T cells, these results indicate the requirement of activation and clonal proliferation of T lymphocytes to produce myelin damage in autoimmune diseases of the PNS.

Animals↗
PubMed1987

[The role of T-lymphocytes in organ-specific autoimmune diseases].

Chronic debilitating diseases such as multiple sclerosis, demyelinating inflammatory polyradiculoneuropathy, rheumatoid arthritis, diabetes mellitus type I, Hashimoto thyroiditis, forms of uveitis and interstitial nephritis, share many characteristics. They are all organ-specific inflammatory diseases of unknown etiology but with strong evidence of tissue-destructive activity of the cellular immune system in the organs respectively affected, i.e. the central or peripheral nervous system, the joints, the islets of Langerhans, the thyroid gland, the retina, or the tubulo-interstitial renal tissue. Recognized animal models of all these diseases are experimentally induced autoimmune conditions that are transferable with autoreactive T-lymphocytes, in contrast to autoantibodies in humoral autoimmune diseases. In recent years, disease-transferring T-lymphocytes, have been successfully grown as lines and clones in vitro, thus finally proving the primary pathogenic role of autoreactive T-lymphocytes in these animal models. Such T-cell lines are valuable tools in further defining autoantigens, studying mechanisms of T-cell activation in vitro, following T-cell migration and organ-specific homing in vivo, and analyzing effector functions in the infiltrated organs. In addition, questions concerning the breakdown of immunological selftolerance and the basic principles of resistance to disease can be addressed, and possibilities of treatment can be approached. Although the basic etiology of the human organ-specific immune diseases is still unknown, these animal models have helped to throw light on some of the pathogenic mechanisms common to these various diseases.

Animals↗
PubMed1986

Astrocytes as antigen-presenting cells. Part II: Unlike H-2K-dependent cytotoxic T cells, H-2Ia-restricted T cells are only stimulated in the presence of interferon-gamma.

Various studies strongly suggest that astrocytes are potent immune-regulating cells. They can be activated to release prostaglandin E, interleukin-1- and interleukin-3-like factors. Cocultivation of antigen-specific T cell lines and astrocytes results in induction of Ia on astrocytes and antigen-specific proliferation of T cells. In the current study, astrocytes were found to be incapable of serving as stimulator cells when unprimed T lymphocytes were used as responders in syngeneic or allogeneic lymphocyte reactions. However, when interferon-gamma (IFN-gamma) was added, astrocytes became Ia positive and potent stimulators in both syngeneic or allogeneic lymphocyte responses. In the presence of IFN-gamma, astrocytes presented antigens to Ia-restricted T hybridoma cells; in contrast hapten was presented to Kb-restricted cytotoxic cloned T cells by astrocytes in the absence of IFN-gamma. Thus, cultured astrocytes do function directly as accessory cells in class I antigen-dependent T cell activation, whereas Ia induction by IFN-gamma is necessary to enable them to present antigen to class II antigen-restricted T cells.

Animals↗
PubMed1986

On the role of astrocytes in polyclonal T cell activation.

Murine astrocytes have been identified to possess accessory cell functions, which are thought to be regulated by the inducible expression of surface Ia molecules. The accessory cell functions include the induction of syngeneic and allogeneic T lymphocyte responses, the cytotoxic T cell activation towards haptens and the antigen-induced stimulation of helper T cell lines. In this report, astrocytes initially being Ia antigen-negative cells were found to restore the phytohaemagglutinin (PHA) response of mouse lymph node cells depleted of accessory cells by treatment with leucin methyl ester (Leu ME). Antisera against Ia determinants did not inhibit the PHA response or the release of interleukin-1 (IL-1) by activated astrocytes. Thus, the presence of Ia antigens is not required for mitogen-induced polyclonal T cell activation. In addition to IL-1 release, astrocytes may favour cell-cell contacts necessary for mitogen-induced polyclonal T cell response.

Animals↗
PubMed1985

Astrocytes as antigen-presenting cells. I. Induction of Ia antigen expression on astrocytes by T cells via immune interferon and its effect on antigen presentation.

Ia antigens seem to control immune responses on at least two levels. First, they influence the antigen recognition repertoire of the T cells. Second, their variable expression on certain antigen-presenting cells is a powerful regulatory mechanism for the local immune reaction. This is particularly important in the central nervous system (CNS) in which no Ia antigens are normally expressed. Recent experiments in this context have shown that astrocytes are able to express Ia antigens during interaction with T cells, and that they function as antigen-presenting cells. The Ia-inducing activity is produced by activated T cells, and can be replaced by immune interferon (IFN-gamma). In this study we report on the functional and kinetic relationship between Ia antigen expression on astrocytes and the immune-specific activation of T cells by astrocytes. Normal resting astrocytes were found to be negative for Ia antigens by immunofluorescence and by biochemical criteria. Moreover, they are only able to stimulate T cells after they have been induced to express Ia antigens by a signal from the T cells, which is probably mediated by IFN-gamma. In conclusion, the immune-specific interaction between astrocytes and T lymphocytes is a sensitively controlled system that might be pivotal to the development of immune responses in the brain. Malfunction of the system could be an important factor in the pathogenesis of aberrant immune reactions in the CNS, e.g., in multiple sclerosis.

Adjuvants, Immunologic↗
PubMed1982

Non-H-2 and H-2-linked immune response genes control the cytotoxic T-cell response to H-Y.

The immunoregulation of cytotoxic T-cell responses to the male-specific antigen H-Y in mice has been found to be genetically controlled by genes of the major histocompatibility complex (H-2). Responsiveness was mainly confined to H-2b strains, but it has also been found in recombinant strains, F1 hybrids, and chimeras that carry at least part of the H-2b haplotype. By using a different immunization procedure it has been shown recently that an H-2k mouse strain (CBA) is also able to mount an equivalent H-Y-specific response. We investigate here, by applying this immunization technique, the responsiveness of other H-2k strains and of strains of other independent H-2 haplotypes. Both responders and nonresponders are found in three haplotypes: k, s, and d. The strain distribution pattern of responsiveness shows a combined influence of non-H-2 and H-2 genes. In certain strains there is a high variability in responsiveness between genetically identical individual animals. We discuss a model of immune response (Ir) gene function which could account for these observations.

Animals↗
PubMed1982

Genetic analysis of the non-H-2-linked Ir genes controlling the cytotoxic T-cell response to H-Y in H-2d mice.

The T-cell mediated immune responses to the male specific minor histocompatibility antigen H-Y in mice have been studied extensively as a model for immune responses to other weak antigens like tumor antigens or autoantigens. In a recent analysis of the strain distribution of the cytotoxic T-cell (Tc-cell) responsiveness to H-Y, it has been found that genes both within and outside the H-2 complex exert an interactive control. Whereas the H-2b strains all are high responders, independent of their non-H-2 background, other H-2 haplotypes (d, k, and s) only allow for a response if they are combined with certain non-H-2 genes. The H-2-linked immune response genes (Ir-genes) have been previously mapped to the I and K or D region of the H-2 complex, but the mapping of the non-H-2 genes has not yet been established. In this study evidence is presented, using recombinant inbred strains and immunoglobulin heavy chain (Igh) congenic strains of mice, to show that there is more than one non-H-2 Ir-gene involved, that the main controlling genes are not linked to the Igh complex, and that at least one non-H-2 Ir-gene is linked to the H-3 region on chromosome 2. This region includes genes for beta-2-microglobulin (beta 2m), the Ly-m11 alloantigen a polymorphic cell surface glycoprotein (Pgp-1), a B-cell specific antigen Ly-4, a transplantation antigen H-3, and genes (Ir-2) controlling the immune response to Ea-1 and H-13.

Animals↗