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Biomedical subjects

B Steiniger

Publications and source records attributed to B Steiniger.

At least 55 records · Page 3Linked to original sources
PubMed1989

Genetic control of rat heart allograft rejection: effect of different MHC and non-MHC incompatibilities.

We investigated the genetic control of heterotopic heart allograft rejection using a family of standard inbred, major histocompatibility complex (MHC)-congenic, and intra-MHC recombinant rat strains. Gene products of the various regions within the rat MHC differed markedly in their capacity to induce rejection. Isolated incompatibility at class I antigens encoded by the RTl.A and RTl.C regions failed to induce rejection within the observation period of 100 days, whereas class II antigens encoded by the RTl.B/D region provoked rapid rejection within 10 days. By comparison of the rejection times of isolated and combined incompatibilities a number of functional interactions could be demonstrated between individual MHC regions which either prolonged or shortened allograft survival. In contrast to rapid rejection of MHC-mismatched heart allografts, differences at non-MHC histocompatibility antigens were associated with graft survival beyond 100 days, although chronic rejection of variable severity was detected histologically. Disparity at non-MHC plus class I antigens, however, provoked acute heart allograft rejection.

Animals↗
PubMed1989

Class II MHC antigens in the rat digestive system. Normal distribution and induced expression after interferon-gamma treatment in vivo.

The normal and interferon-gamma induced expression of class II MHC antigens was investigated immunohistologically in the digestive system of LEW rats. In the normal state class II molecules were present in interstitial dendritic cells, B lymphocytes and epithelial cells. Epithelial class II expression was restricted to enterocytes in certain portions of the small intestine and to some duct epithelia in salivary glands. After continuous intravenous infusion of interferon-gamma (IFN-gamma) for 3 days, class II MHC antigens were induced in large vessel endothelium and in the surface epithelia of the tongue, oesophagus and proventricle. In the gastric glands class II molecules appeared in mucous neck cells and in parietal cells, while adjacent mucous surface cells and chief cells did not acquire class II reactivity. All enterocytes, including the previously negative colonic epithelium, were induced to express class II antigens. In the salivary glands class II antigens appeared in all duct epithelia. Serous acinar cells were induced in the parotids, but in the submandibular glands and in the pancreas the serous gland epithelium stayed negative. Our study thus shows that the effects of IFN-gamma on class II MHC antigen expression in vivo depend on the differentiation pathway of the individual cell. The normal distribution in rats suggest that class II MHC antigens may play a role in peptide transport across specialized epithelia. It remains to be determined whether such a function is enhanced after IFN treatment.

Animals↗
PubMed1988

Interferon-gamma in vivo. Induction and loss of class II MHC antigens and immature myelomonocytic cells in rat organs.

The effects of recombinant rat interferon-gamma on class II major histocompatibility complex antigen expression in vivo were studied by immunohistology in LEW rats after continuous intravenous infusion for three days. Interferon-gamma administration led to a systemic induction of class II molecules in previously negative parenchymal and stromal cells. The induction patterns observed were highly reproducible, but not closely dose dependent within a 25-fold dose difference tested. However, the effect of interferon infusion differed profoundly in individual cell types, and appeared to be related to the differentiation stage of each cell population. Thus, epithelial cells like duct epithelia, urothelium or basal ear skin keratinocytes as well as endothelia in big vessels were strongly and easily induced for class II antigen expression. Parenchymal cells like cardiomyocytes and hepatocytes showed intermediate reactivity, while capillary endothelia, neurons in the brain, straight proximal kidney tubules or endocrine pancreatic islet cells did not express class II antigens. The induced expression was rapidly lost from most cells within one or two days after interferon withdrawal; the only exception occurred in keratinocytes. Long-term alterations were, however, still found 14 days after infusion. Interstitial class II-positive dendritic-shaped cells were increased in the organs and hepatic Kupffer cells carried class II antigens. On conventional histology all organs appeared perfectly normal at this date. After three days of interferon, cells of an immature myelomonocytic phenotype occluded medium-sized and small veins in all organs and occurred in granuloma-like lesions in the liver. Although these cells quickly disappeared after interferon withdrawal they might have been at least partially responsible for single deaths on day three. Our study provides a basis for testing the immunological in vivo function of parenchymal class II antigen expression and its differentiation-specific regulation.

Animals↗
PubMed1988

Rat ependyma and microglia cells express class II MHC antigens after intravenous infusion of recombinant gamma interferon.

Recombinant rat gamma-interferon was administered to Lewis rats by continuous intravenous infusion. After a 3-day administration period, at various dosages, a constant pattern of class II major histocompatibility complex (MHC) antigen induction was found in the brains and cerebella. Immunohistological double staining for class II antigens and glial fibrillary acidic protein showed that the majority of newly induced cells were microglia. The endothelium of large blood vessels and ependymal cells also expressed class II antigens. These findings demonstrate that systemically raised interferon levels can affect MHC antigen expression in the brain. Astrocytes are obviously not the primary cell type to acquire class II reactivity, and thus potential antigen-presenting capacity, in this situation.

Animals↗
PubMed1986

Ia antigens in plastic-embedded tissues: a post-embedding immunohistochemical study.

The aim of the present study was to establish a plastic embedding technique that makes possible the immunohistochemical demonstration of class II major histocompatibility complex (MHC) antigens (Ia antigens) in undecalcified joint tissues. Therefore a series of fixatives and dehydrating agents was tested for saving Ia immunoreactivity by post-embedding immunostaining of thin sections (2 microns) of rat tissues that had been embedded in glycol methacrylate (GMA), and by comparing with cryostat sections. An indirect immunoperoxidase and the avidin-biotin complex (ABC) technique were used. Combined with fixation by 4% formaldehyde, dehydration with GMA was found to give the best preservation of Ia antigenicity, followed by dehydration with ethylene glycol. The thinness of tissue sections facilitated the association of Ia antigens with different subcellular compartments in distinct cell populations. These various patterns are described.

Animals↗