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F H Claas

Publications and source records attributed to F H Claas.

257 records · Page 15Linked to original sources

ABH antibodies causing platelet transfusion refractoriness.

Two alloimmunized patients with multispecific anti-HLA and high-titered ABH antibodies showed transfusion failures after ABH-mismatched HLA-identical platelet transfusions, whereas ABH-matched HLA-identical platelets showed sufficient increments. The anti-A and -B could be demonstrated on platelets by immunofluorescence tests using FITC-labeled goat anti-human IgG. These platelet antibodies could be absorbed with red cells and platelets of the appropriate ABH type. In contrast to previous reports about the influence of ABH antibodies on platelet survival, not only a proportion of the platelet population were destroyed after infusion, but almost all ABH-incompatible platelets were destroyed.

ABO Blood-Group System↗

Influence of non-H-2 genes on the in vivo response to penicillin-treated autologous platelets.

Mice of different inbred strains were injected intravenously on day 0 and day 6 with autologous platelets incubated in a penicillin solution. After the second injection mice of most strains died immediately with anaphylactic symptoms. Both passive transfer experiments and indirect immunofluorescence studies suggest that a serum factor (probably IgM) is involved in this phenomenon. Only mice with a C3H background were unable to respond to autologous penicillin-treated platelets, although C3H platelets did induce a lethal response in B10.A mice. Experiments in which B10.A mice were primed with autologous penicillin-treated platelets and rechallenged with allogeneic penicillin-treated platelets, showed that the response is directed against a polymorphic non-H-2 antigen in combination with penicillin.

Animals↗

Ultrastructural localization of HLA-DR and HLA-DQ molecules in Langerhans cells and B cells: an immunoelectronmicroscopic study.

Using the immunoelectronmicroscopic techniques of Lowicryl embedding and ultracryomicrotomy, the intracellular distribution of HLA class II molecules was investigated on a human B cell line and on human Langerhans cells. These techniques enabled us to localize the HLA class II molecules on fixed specimens in which mobilization or clustering induced by cross linkage with antibodies is ruled out. Compared with Lowicryl embedding, the ultracryomicrotomy clearly showed more labeling. Both in B cells and Langerhans cells, the HLA-DR molecules were predominantly found in intracellular vesicular structures and on the plasma membrane. The HLA-DQ molecules were less abundant than HLA-DR molecules in the B cells and Langerhans cells. In the B cells, HLA-DQ molecules were found on the plasma membrane and in the cytoplasm. In the Langerhans cells, some HLA-DQ molecules were also found in intracellular vesicular structures. These experiments show a different localization of HLA-DR and -DQ antigens both in Langerhans cells and B cells, suggesting a different function for these molecules. The localization of HLA-DR molecules may indicate that these molecules take part in the recycling process of the plasma membrane in B cells and Langerhans cells. The HLA-DQ molecules are not internalized or recycled by the B cells, and a limited internalization of these molecules takes place in Langerhans cells. Finally, no HLA class II or clathrin molecules were found on the Birbeck granules, suggesting that, when no cross-linking with antibodies takes place, Birbeck granules, suggesting that, when no cross-linking with antibodies takes place, Birbeck granules do not play a role in recycling of HLA class II molecules in Langerhans cells.

Antibodies, Monoclonal↗

A molecular mechanism of T cell downregulation by blood transfusion.

Pretransplant blood transfusions have been given to renal transplant recipients in order to improve graft survival since almost 20 years. Nevertheless, the mechanism involved in this tolerating effect of blood transfusions has not been revealed yet. Recent data, showing a need for sharing of at least one HLA-DR antigen between blood transfusion donor and recipient to obtain downregulation of the alloimmune response, are the basis of the present hypothesis. We postulate that HLA-DR-shared blood transfusions activate CD4+ T cells recognizing allogeneic peptides in the context of the shared HLA-DR molecule. These CD4+ T cells are able to downregulate the immune response of autologous activated (thus HLA-DR-positive) T cells directed against any allogeneic organ, sharing at least one allogeneic peptide with the blood transfusion donor. Essential in this hypothesis is that the T cells activated by the graft will pick up that allogeneic peptide from the transplanted organ and present it in the context of the shared HLA-DR molecule to the autologous regulatory CD4+ T cells, primed by the blood transfusion.

Animals↗

Different patterns in donor-specific production of T-helper 1 and 2 cytokines by cells infiltrating the rejecting cardiac allograft.

BACKGROUND: Cytokines play an important role in allograft rejection. The local production of cytokines by T-helper 2 cells within an allograft could influence the induction of graft rejection. METHODS: Therefore we studied the in vitro production of cytokines by cells infiltrating the graft. graft-infiltrating cell cultures derived from human endomyocardial biopsy specimens more often produced interleukin-2 (p < 0.001), interferon-gamma (p < 0.001), interleukin-4 (p = 0.02), and interleukin-6 (p = 0.04) after stimulation with a B-cell line obtained from the heart donor than after stimulation with a third-party B-cell line. Furthermore, the levels of these cytokines were significantly higher after donor stimulation than after third-party stimulation (p < 0.001). RESULTS: Within the first 90 days after heart transplantation, significantly higher levels of interleukin-2 (p = 0.050 and interferon-gamma (p = 0.02) were produced by donor-stimulated lymphocyte cultures derived from biopsy specimens taken during a rejection episode compared with cultures from biopsy specimens taken during a period without rejection. After 90 days, the levels of T-helper 1 cytokine (interleukin-2 and interferon-gamma) production were, irrespective of the rejection grade, comparable with those found in the cultures from rejection biopsy specimens taken early after transplantation. With regard to T-helper 2 cytokines (interleukin-4 and interleukin-6), no relation was found with the presence of rejection at any time after transplantation. CONCLUSIONS: These data suggest that in the first 3 months after heart transplantation, acute rejection is associated with the production of increased levels of T-helper 1 cytokines but not of T-helper 1 cytokines but not of T-helper 2 cytokines by donor stimulated graft-infiltrating lymphocytes. Thereafter, the T-helper 1 cytokine production of graft-infiltrating lymphocytes remained high, suggesting a continuous state of immunologic activity even in the absence of rejection.

B-Lymphocytes↗