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Sökning: WFRF:(Böhme Jan)

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1.
  • Brenden, N., et al. (författare)
  • Differential MHC expression requirements for positive selection of separate TCR Vb families
  • 1999
  • Ingår i: Immunogenetics. - 0093-7711 .- 1432-1211. ; 49:1, s. 1-6
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Positive selection has been proposed to be involved in protection from diabetes. We examined positive selection by fluorescence-activated cell sorter analyses in thymocytes of protected and susceptible E-transgenic and non-transgenic NOD mice. Three Vb families showed positive selection in E-transgenic mice. Vb6+CD4+ and Vb10+CD4+ thymocytes were found at higher frequencies in both protected NOD-Ea and susceptible NOD-DY mice. The increased frequencies of Vb13+CD8+ thymocytes were found in protected NOD-Ea mice only, and not in susceptible NOD-DY transgenic mice. These three Vb families were further examined in bone-marrow chimeras between NOD-Ea and non-transgenic NOD mice, where we could examine the contribution of E-expressing bone-marrow-derived cells in positive selection. We find that NOD-Ea→NOD-Ea chimeras have an increased positive selection of Vb13+CD8+ cells and that positive selection is more efficient when both thymic epithelium and bone-marrow-derived cells express the E molecule. This was also seen for Vb6+CD4+ cells. However, for Vb6, bone-marrow-derived cells alone were also capable of positive selection. Positive selection of Vb10+CD4+ cells was restricted to E-expressing thymic epithelium only. For Vb13+CD8+ cells, we found that positive selection is most efficient with E-expression on both thymic epithelium and bone-marrow-derived cells, although positive selection also occurs with E-positive epithelium only. For Vb6+CD4+ cells, the dominating selecting cells are bone-marrow-derived cells, and Vb10+CD4+ cells seem to be selected exclusively by the thymic epithelium. Thus, the conditions for positive selection seem to vary considerably between different Vb families.</p>
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2.
  • Brenden, N., et al. (författare)
  • Disease-protected major histocompatibility complex Ea-transgenic non- obese diabetic (NOD) mice show interleukin-4 production not seen in susceptible Ea-transgenic and non-transgenic NOD mice
  • 1998
  • Ingår i: Immunology. - 0019-2805 .- 1365-2567. ; 95:1, s. 1-7
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>The non-obese diabetic (NOD) mouse is an animal model for insulin- dependent diabetes that has many similarities to the human disease. NOD mice transgenic for the Ea gene, allowing expression of the E molecule, are protected from diabetes and rarely develop insulitis. An Ea transgene mutated in the promoter region, (ΔY) lacks E expression on most B cells, thymic medullary epithelium and primary antigen-presenting cells, and confers no protection whatsoever. We have used these transgenic NOD mice, together with non-transgenic NOD mice, to study the correlation of E expression and production of interleukin-4 (IL-4) and interferon-γ (IFN-γ). We show that protected E-transgenic NOD mice have elevated levels of IL-4 compared with non-transgenic mice, both in the thymus and in the periphery. However, susceptible ΔY-transgenic mice have elevated thymic IL-4 levels, but express almost as little IL-4 as non-transgenic NOD mice in the periphery. This drop in peripheral IL-4 production seen in ΔY-transgenic mice thus correlates with the decreased E expression in the periphery of ΔY-transgenic NOD mice. In contrast, there were no differences in IFN-γ production between the three NOD lines. We suggest that Ea-transgenic NOD mice have E-selected regulatory T cells producing IL-4, which are subsequently activated by E-expressing primary antigen-presenting cells in the periphery. This activation would then be instrumental for the E-mediated protection from disease in NOD mice. Such a process would explain the total absence of protection in ΔY-transgenic NOD mice, despite their widespread E expression.</p>
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3.
  • Brenden, N., et al. (författare)
  • E expression is needed on both bone marrow derived cells and thymic epithelium to increase IL-4 production and achieve protection in NOD bone marrow chimeras
  • 1999
  • Ingår i: Cytokine. - 1043-4666 .- 1096-0023. ; 11:10, s. 766-772
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>The NOD mouse is an animal model for insulin-dependent diabetes with many similarities to the human disease. NOD mice which are transgenic for the Ea gene, allowing expression of the E molecule, are protected from diabetes and rarely develop insulitis. We have constructed bone marrow chimeras between transgenic and non-transgenic NOD mice to study the correlation of E expression on bone marrow derived cells and thymic epithelium vs the production of IL-4 and IFN-γ. We show that NOD-E→NOD-E and NOD-E→NOD chimeras have elevated levels of IL-4 compared to NOD→NOD and NOD→NOD-E chimeras in the thymus. However, in the periphery the protected NOD-E→NOD-E show much higher IL-4 levels than any of the other chimeras. This drop in peripheral IL-4 production seen in NOD-E→NOD, NOD→NOD-E and NOD→NOD chimeras correlates with the increased insulitis seen in these mice compared to NOD-E→NOD-E. In contrast, there were no differences in IFN-γ production between the chimeras. We suggest that the precommitted, regulatory T cells, selected in an E-expressing thymic environment, need continuous interaction with E-expressing primary antigen presenting cells in the periphery for optimal IL-4 production. Decrease in IL-4 production correlates with increased insulitis.</p>
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5.
  • Böhme, Jan, et al. (författare)
  • Human class II major histocompatibility antigen β-chains are derived from at least three loci
  • 1983
  • Ingår i: Nature. - Nature Publishing Group. - 0028-0836. ; 301:5895, s. 82-84
  • Tidskriftsartikel (refereegranskat)abstract
    • Class II antigens of the major histocompatibility complex (MHC) consist of two glycosylated, membrane-integrated polypeptide chains1. These cell surface-expressed molecules are involved in several immunobiological events involving cell-cell interactions2,3, most of which seem to require that genetically identical class II antigens, or other molecules controlled by the same region of the MHC, are expressed on the interacting cells4. The extensive genetic polymorphism of the class II antigens5 has rendered analyses in the human system of the number of non-allelic species of class II antigens difficult, although several laboratories have reported the existence of at least two types of human class II antigens6-9. Here we present the results of experiments using restriction enzyme digestions and separation of DNA from individuals homozygous for the MHC followed by hybridization to human class II antigen α-10,11 and β-12-14 chain cDNA probes. While the α -chain probe gave only a single hybridization band, the various β -chain probes revealed a more complex pattern that is consistent with the existence of at least three separate β -chain genes or pseudogenes in the human MHC.
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9.
  • Högstrand, K., et al. (författare)
  • DNA damage caused by etoposide and γ-irradiation induces gene conversion of the MHC in a mouse non-germline testis cell line
  • 1999
  • Ingår i: Mutation research. - 0027-5107 .- 1873-135X. ; 423:1-2, s. 155-169
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>We have explored the effects of γ-irradiation and etoposide on the gene conversion frequency between the endogenous major histocompatibility complex class II genes Abk and Ebd in a mouse testis cell line of non-germline origin with a polymerase chain reaction assay. Both γ-rays and etoposide were shown to increase the gene conversion frequency with up to 15-fold compared to untreated cells. Etoposide, which is an agent that stabilise a cleavable complex between DNA and DNA topoisomerase II, shows an increased induction of gene conversion events with increased dose of etoposide. Cells treated with γ-rays, which induce strand breaks, had an increased gene conversion frequency when they were subjected to low doses of irradiation, but increasing doses of irradiation did not lead to an increase of gene conversion events, which might reflect differences in the repair process depending on the extent and nature of the DNA damage. These results where DNA damage was shown to be able to induce gene conversion of endogenous genes in mouse testis cells suggests that the DNA repair system could be involved in the molecular genetic mechanism that results in gene conversion in higher eukaryotes like mammals.</p>
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10.
  • Högstrand, K, et al. (författare)
  • Gene conversion of major histocompatibility complex genes in the mouse spermatogenesis is a premeiotic event
  • 1997
  • Ingår i: Molecular Biology of the Cell. - 1059-1524 .- 1939-4586. ; 8:12, s. 2511-2517
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>The molecular genetic mechanism of gene conversion in higher eukaryotes remains unknown. We find it of considerable interest to determine when during spermatogenesis gene conversion occurs. We have therefore purified pachytene spermatocytes and haploid spermatocytes from adult mice and analyzed these fractions for the presence of gene conversion products resulting from the transfer between the major histocompatibility complex class II genes Ebd and Abk in a polymerase chain reaction assay. We have further isolated spermatogenic cells from prepubescent mice and analyzed them for the presence of the same gene conversion products. We can detect gene conversion products in testis cells as early as in 8-d-old mice where the only existing spermatogenic cells are spermatogonia. The frequency of gene conversion products remains the same as the cells reach meiosis in 18-d-old mice, and is unchanged after meiosis is completed in haploid spermatocytes. Gene conversion of this specific fragment therefore appears to be a premeiotic event and, consequently, relies on genetic mechanisms other than normal meiotic recombination.</p>
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