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Notizen: In-vitro-cultured bursal epithelium (BE) and BE-conditioned medium (BECM) induce B-L antigen on chicken intraembryonic cells. Cells prepared from 9-day-old intraembryonic mesoderm were fractionated in accordance with cell size by linear albumin gradient sedimentation at 1 g. Two cell types could be distinguished on which expression of the B-L antigen was altered after a 6-h incubation with the bursal epithelial component. One fraction contained small mononuclear cells with low sedimentation velocity (≤ 3 mm/h) and low spontaneous proliferation activity. These cells responded strongly to BECM and showed a slight but not significant response to BE (index after incubation with BECM 3.8, with BE 1.7, as compared with RPMI medium control). The other fraction was composed of large mononuclear cells with sedimentation velocity 〉 9 mm/h and with high spontaneous proliferation. These cells showed a response of equal magnitude to both BE and BECM (index after incubation with BE 2.0, with BECM 2.3). These results suggest that the bursa of Fabricius has influence on two different cell types: a large, probably primitive undifferentiated cell, responding equally to bursal cellular contacts and BE culture supernatant, and a small mononuclear cell type, probably more mature, responding more clearly to the bursal humoral factor.

Notizen: MHC class-I antigens on peripheral blood macrophages and bursa cells were analysed after adoptive bursa cell transfer to cyclophosphamide-treated immunodeficient chickens. We studied the expression of B-F locus-encoded antigens (B-F is homologous to mouse H-2K, D) on macrophages and B cells and found that macrophage B-F antigens are of host origin, whereas bursa cells express only donor-type B-F antigens. Both syngeneic and allogeneic bursa cells restored IgM antibody production to a T-cell-independent antigen, Brucella, but only syngeneic bursa cells could restore the IgG antibody response to a thymus-dependent antigen, sheep erythrocytes. The results indicate that B-cell maturation and macrophage-B-cell interaction are not MHC-restricted but that a restriction exists in T-cell-B-cell collaboration.

Notizen: Background and aims: In coeliac disease, the gut involvement is gluten-dependent. Following the introduction of a gluten-free diet, inflammatory cell infiltration decreases in the small intestinal mucosa. Our hypothesis was that the oral mucosa might mirror the changes found in coeliac disease similarly to the mucosa of the small intestine. Thus, the number of inflammatory cells in the oral mucosa would decrease in patients with coeliac disease on a gluten-free diet. Methods: The distribution CD45RO+ and CD3+ T cells, T-cell subpopulations (CD4+ , CD8+ , T-cell receptor (TCR)αβ+ and TCRγδ+ cells) and HLA DR expression were studied in the buccal mucosa of 15 untreated and 44 gluten-free diet treated coeliac disease patients, and of 19 controls. All 15 patients with untreated coeliac disease were immunglobulin (Ig)A endomysial antibody positive and all 44 patients on gluten-free diet except one were endomysial antibody negative, as were all control subjects. Results: Untreated coeliac disease patients did not differ from controls in the densities of CD45RO+ cells, CD3+ cells or of T-cell subsets. In contrast, in treated coeliac disease patients, a significant increase in the numbers of mast cells, CD3+ and CD4+ lymphocytes was found in the lamina propria of oral mucosa as compared with patients with untreated coeliac disease and controls. The increase in CD3+ T cells was in part owing to an increase in lymphocytes expressing no TCR. No differences were found in the expression of human leucocyte antigen (HLA) DR in the epithelium or in the lamina propria in the patient groups studied or in the controls. In treated coeliac disease patients only a few TCRγδ+ T cells were found intraepithelially and in the lamina propria, but these cells were not detected in the lamina propria of oral mucosa of patients with untreated coeliac disease or in the controls. Conclusions: The infiltration of T cells into oral mucosa was increased in treated coeliac disease patients in spite of adherence to a gluten-free diet. Because the CD3+ T cell count was higher than those of the TCRαβ+ and TCRγδ+ T cells, there must be other cells involved, probably natural killer (NK) cells. The increase in T-cell subsets in the treated coeliac disease patients seems not to result from poor dietary compliance, but might occur as a late immune response in coeliac disease and reflect chronic immunologic stimulation followed by regeneration of memory T cells.

Notizen: After transplantation of bursal stem cells into cyclophosphamide-treated newly hatched chicks, the first lymphoid cells in the spleen of the recipients were observed on the first day after the cell transfer and the first plasma cells on day 3. The repopulation of the Schweigger-Seidel sheaths started from their periphery on day 6. The first germinal centers were detected 20 days after the cell transfer. In cyclophosphamide-treated birds without cell transplantation, only the periphery of the Schweigger-Seidel sheaths became repopulated, and no plasma cells or germinal centers were observed. The results indicate that already at the age of 3 days the bursa contains some cells of postbursal maturity, able to home to the spleen.

Notizen: The ontogeny of alkaline phosphatase in the bursa of Fabricius was Studied by histochemical and biochemical methods. According to the quantitative determinations, the activity of alkaline phosphatase increased from the 11th to 17th day of incubation—that is, during the time of the lymphoid follicle formation in the developing bursa. The activity was localized in the mesenchymal tissue surrounding the lymphoid follicles. Testosterone given in ova prevented the appearance of alkaline phosphatase in the bursal mesenchyme but had no effect on the activity of the embryonic liver. In contrast, in ova treatment with cyclophosphamide had no effect on the alkaline phosphatase in the bursa. By using transplantation of embryonic bursal stem cells, it was further shown that, in contrast to cyclophosphamide, testosterone destroys the capacity of the bursa to serve as a differentiation site for the B-cell lineage. The results indicate that testosterone affects the stromal cells of the bursa, whereas cyclophosphamide destroys only the lymphoid population undergoing differentiation and leaves the bursal stroma intact.

Notizen: Activation of T lymphocytes by an antigen requires joint recognition of the- antigen and the class-H HLA determinants on the membrane of the antigen-presenting cells (APC). Patients with reactive arthritis exhibit a depressed lymphocyte transformation response 10 Yersinia, suggesting a possible immunoregulatory disturbance in these patients. In this study the role of Ia (dass-II HLA antigen)-positive APC in the lymphocyte response to a complex antigen, whole Yersinia bacterium, was evaluated. The results demonstrate that Ia-positive cells are necessary for the T-lymphocyte response to Yersinia. The role of APC in the pathogenesis of reactive arthritis is discussed.

Notizen: The immunological status of seven patients with disseminated melanoma during BCG scarification was followed. As parameters, the total peripheral blood leukocyte and lymphocyte counts, serum immunoglobulin levels, natural ABO blood group antibodies, lymphocyte responses in vitro to PHA and PPD, and skin reactivity against PPD and candidin were followed during a period of 2-36 months. The EAC-rosette-forming cells increased and the E-rosette-forming cells decreased during prolonged BCG therapy. The skin reactions and lymphocyte responses showed in most patients conversion from negative to positive or augmentation at the start of the therapy. Later on, however, the values in most patients dropped before disseminated disease became clinically apparent. In the only surviving patient the values first increased, remained high, and after 100 weeks treatment decreased. After 140 weeks'treatment immunological parameters are similar to pre-treatment levels. The possibility that prolonged intensive BCG treatment might eventually suppress the immune system, and thus result in an enhanced risk of dissemination of the disease, is discussed.

Notizen: We found that chickens responded to an injection of 1 mg of alum-precipitated conjugates of (4-hydroxy-3-iodo-5-nitrophenyl)acetyl and bovine serum albumin (NIP-BSA) or human gammaglobulin (NIP-HGG) with an anti-NIP response. This response was enhanced to fivefold titers if the birds were given a small dose (2 or 0.2 μg) of the carrier protein in complete Freund's adjuvant a week before injection. If the dose of the carrier was large (200–2,000 μg), it decreased the subsequent anti-NIP response to the conjugate. The effect of the preimmunization correlated with the formation of anti-carrier antibodies: a good anti-carrier response was connected with inhibition and a poor anti-carrier response with enhancement of the anti-NIP response. Large preimmunization doses of the carrier caused enhanced anti-hapten responses if the carrier was methylated or dodecanoylated; in this case the anti-carrier humoral responses were weak. Large doses of the native carrier increased the subsequent anti-hapten response if spleen cells of the preimmunized donors were injected into cyclophosphamide-treated donors, who were then immunized with the hapten conjugate. The results confirm earlier studies indicating that collaboration of carrier-specific cells and hapten-specific cells is required in the chicken for an optimal anti-hapten response. They further indicate that carrier-primed cells do not reside in the thymus and that, also in birds, immunization by methylated or dodecanoylated protein causes good priming for helper function but bad priming for the antibody formation against the protein.

Notizen: Cells from chickens bursectomized at 60 h of incubation (Bx) are known lo produce immunoglobulins without any detectable antibody specificity. In the present work cells from Bx birds were cultured together with bursal epithelial cells (BE) or bursal epithelium-conditioned medium (BECM) to establish whether they could be induced to produce specific antibodies. Cells obtained from 10-day-old or 10-week-old birds were used. The effects were assessed with regard to the production of total immunoglobulins and specific antibodies; the birds had been preimmunized. BE had no effect on the production of immunoglobulins by either Bx or control (Co) cells. When cells from 10-week-old birds were cultured in the presence of BECM, no difference in the immunoglobulin production was seen between Bx and Cochicken cells. At the age of 10 days the cells of Bx birds produced considerably less Ig than the cells of normal Co birds. At this age BECM had no effect on the Co cells, but it markedly enhanced the production of IgA-class immunoglobulins of Bx birds. With regard to production of specific anti-tetanus antibodies, BE stimulated the production of IgA-class antibodies by cells from preimmunized Co chickens but had no effect on cells from preimmunized Bx birds. In spite of the normal production of immunoglobulins in vitro the cells of Bx chickens did not produce specific antibodies. In conclusion, these findings indicate that if B cells have matured without a contact with the bursa of Fabricius, later in vitro exposure to BE or BECM can no longer induce them to production of specific antibodies.