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Biomedical subjects

D Wernet

Publications and source records attributed to D Wernet.

At least 37 records · Page 2Linked to original sources
PubMed1994

Reactivation of antibodies of donor and recipient origin to platelet antigens early after allogeneic bone marrow transplantation: a case report.

Reactivation of platelet-reactive antibodies of donor and recipient origin is described in a patient following allogeneic BMT (donor: anti-HPA-5b; recipient: anti-HLA, anti-HPA-1b). The antibodies were detected around day 15 after BMT, peaked around day 25, and then decreased. These antibodies are interpreted as an antigen-independent reactivation of secondary B-cell responses, activated in the context of recognition of host antigens by the graft.

Adult↗
PubMed1994

A simple technique for red blood cell removal in major ABO-incompatible bone marrow transplantation.

A simple technique for red blood cell (RBC) removal in major ABO-incompatible bone marrow transplantation is reported requiring two centrifugation steps, special blood bags and a mechanical device to separate the buffy coat from RBCs within the bag. In 42 transplantations an average of 84% of nucleated cells was recovered with an average contamination of 7.5 ml packed RBCs. The preparations were well tolerated in all patients whose isoagglutinin titers had not been reduced. Bone marrow engraftment was not significantly different from control groups.

Adult↗
PubMed1994

[Demonstration of platelet-specific alloantibodies in HLA-sensitized hematologic oncologic patients].

Alloimmunization to the platelet-specific antigen systems HPA-1, -3 and -5 was studied in 59 multitransfused patients (31 females, 16 males, 12 children) with haematologic-oncologic disorders. All patients tested had broad-reacting or multispecific HLA antibodies. Of these, 10 (17%) were found to have additional platelet-specific alloantibodies. With respect to HLA sensitization, 9 out of 10 platelet-specific alloantibodies were found in sera which showed HLA antibodies reacting with more than 95% of unselected panel cells. Determination of antibody specificity revealed 6 patients with anti-HPA-1b, one patient with anti-HPA-3a, and 2 patients with anti-HPA-1b combined with anti-HPA-3a. One patient had anti-HPA-5b; in retrospect, only the HPA-5b antibody was demonstrable before the beginning of transfusion therapy and before HLA sensitization.

Adult↗
PubMed1993

Serological screening, using three different test systems of platelet-transfused patients with hematologic-oncologic disorders.

Sera of hematologic-oncologic patients were tested regularly after platelet transfusions in three test systems: lymphocytotoxicity test, platelet adhesion immunofluorescence test, and--only selected sera--in the monoclonal antibody-specific immobilization of platelet antigen test. Of 388 patients 53 (14%) had HLA antibodies 5 of these in combination with platelet-specific alloantibodies. Lymphocyte-restricted (non-HLA) reactions were observed in 20 patients, the majority of which was attributed to lymphocyte-specific auto- or alloantibodies. Sera of 27 patients showed platelet-specific reactions, usually cold-reacting autoantibodies which have no effect in vivo.

Adult↗
PubMed1992

Isoagglutinins following ABO-incompatible bone marrow transplantation.

Isoagglutinins were investigated following ABO-incompatible bone marrow transplantation. In major incompatibility anti-A tends to require more time to disappear than anti-B. Correspondingly, A erythrocytes require more time to become demonstrable. There is no such difference in major plus minor incompatibility. In minor incompatibility, isoagglutinins against the recipient blood group may be produced early after bone marrow transplantation, which then give way to a possibly lifelong tolerance for the recipient's old blood group.

ABO Blood-Group System↗
PubMed1992

[Isoagglutinins after bone marrow transplantation with minor ABO incompatibility].

Sera of 22 patients after BMT with blood group change from A to 0 were investigated. Early after BMT 59% of the patients developed a temporary anti-A whereas late after BMT none of the patients tested showed isoagglutinins against A even though the red blood cells were of type 0 and anti-B was present. The onset of these anti-A isoagglutinins correlated with production of leukocytes by the donor BM and is regarded as a sign of GvHR. Late after BMT a permanent immunological tolerance to the A antigen of the recipients' old blood group seems to exist.

ABO Blood-Group System↗
PubMed1990

[ABO-major incompatible bone marrow transplantation. Experiences with a simple method for the preparation of erythrocyte-poor bone marrow].

The special preparative technique presented here, used in ABO-major-incompatible BMTs, enables an excellent stem cell yield (mean: 94%), reducing the number of incompatible RBCs to a minimum (mean: 3.5 ml packed RBCs). This easy procedure is performed by simple mechanical means, using a pair of opposed, specially formed yaws and a modification of a common blood-collecting bag.

ABO Blood-Group System↗
PubMed1982

Genetic regulation of the antibody response to H-2Db alloantigens in mice. V. Control by several genes of the H-2 complex in mice of the C57BL/10 background.

The cytotoxic antibody response to the H-2Db alloantigen has been investigated in ten strains of the C57BL/10 background. Three types of responses could be distinguished: no detectable response, an IgM response, and an IgG response. The IgG response is influenced by the D and probably the I-A region of the H-2 complex, whereas the IgM response is dependent on the allele for the E beta chain. The hypothesis is proposed that regulatory T cells, which recognize the antigen in context of self MHC molecules, determine the outcome of an anti-H-2Db immunization in which the I-E molecule restricts the IgM response; the D molecule is probably responsible for activation of suppressor T cells which suppress only the IgG response.

Animals↗
PubMed1982

Genetic regulation of the antibody response to H-2Db alloantigens in mice. IV. Antigens that activate helper T cells for IgG, coded for by the non-H-2 genome.

When B10.A(5R) mice are immunized with congenic C57BL/10 cells only 2-ME-sensitive antibodies (IgM type) are found directed against H-2Db. To obtain 2-ME-resistant antibodies (IgG type) 5R mice must be immunized with noncongenic cells (e.g., A.BY); in this case non-H-2 cell surface antigens will activate helper T cells to induce anti-Db IgG antibody production by B cells. An attempt was made to define helper antigens that activate helper T cells. Neither N-2 antigens of seven H-2Db recombinant strains nor a limited set of non-H-2 cell surface antigens were able to serve as helper antigens. By using individual backcross mice as antigen, one helper antigen was found on the background of strain A under the conditions used, whereas other backgrounds may carry more than one antigen. The helper antigen is dominantly expressed in F1 mice and has to be presented on the same cell as H-2Db to induce the switch from IgM to IgG.

Animals↗
PubMed1981

Cell-mediated lympholysis in H-2K/D identical congenic strain combinations.

Eight H-2K/D identical congenic strain combinations were tested in cell-mediated lympholysis. The reaction pattern of selected mouse strains revealed unidirectional reactivity to Tla-linked antigens in six strain combinations, whereas in two strain combinations the loci coding for the target antigen could only tentatively be linked to H-2. The Tla-linked loci defined by the different strain combinations appear to be identical with the H-2T (Qa-1) locus. Typing of B10.W lines for the H-2T (Qa-1) locus revealed the presence of alleles that appear to be the same as those present in inbred strains, as well as alleles that are different from the inbred-defined alleles but that share some determinants with the latter. The H-2T (Qa-1) system thus appears to consist of a limited number of alleles, some of which are closely related and presumably similar in their genetic structure.

Animals↗
PubMed1980

Genetic control of T-cell proliferative responses to poly(glu40ala60) and poly(glu51lys34tyr15): subregion-specific inhibition of the responses with monoclonal Ia antibodies.

The relationship between Ir genes and Ia antigens was studied in the T-cell proliferative responses to two synthetic polypeptides poly(glu40ala60) (GA) and poly(glu51lys34tyr15) (GLT15). The response to GA was found to be controlled by an Ir gene in the I-A subregion, whereas the anti-GLT15 response was shown to be under dual control, one Ir gene mapping probably in the I-A subregion, and the other in the I-E subregion. We obtained two different lines of evidence suggesting identity of Ir and Ia genes. First, the presence of certain serologically identified allelic forms of the I-A-encoded A molecule correlated with the responder status to GA both in inbred strains and in B10.W lines, the latter carrying wild-derived H-2 haplotypes. Thus the Ir and Ia phenotypes were not separable in strains of independent origin. Second, the anti-GA response was completely inhibited by monoclonal antibodies against determinants on the A molecule (Ia.8, 15, and 19), but not by a monoclonal antibody against a determinant on the E molecule (Ia.7). In contrast, the anti-GLT15 response was only inhibited by a monoclonal antibody against the E molecule, but not by antibodies against the A molecule. Our data support the hypothesis that Ia antigens, as restriction elements for T-cell recognition, may in fact be the phenotypic manifestation of Ir genes.

Alanine↗
PubMed1976

Genetic regulation of the antibody response to H-2Db alloantigens in mice. III. Inhibition of the IgG Response to noncongenic cells by preimmunization with congenic cells.

When B10.A (5R) mice (H-12i5) are immunized with spleen cells from congenic B10 mice (H-12b), they respond to alloantigens of the H-2Db region by producing antibodies of only IgM type. In contrast, they produce both IgM and IgG antibodies when immunized with A.BY cells (H-2b) that carry other foreign cell surface antigens (non-H-2) in addition to H-2Db. Preimmunization of 5R mice with two injections of congenic cells leads to an H-2Db specific inhibition of the IgG response to a subsequent immunization with A.BY cells. It is concluded that congenic B10 cells fail to activate helper T cells which are necessary to induce the switch from IgM to IgG production. Instead T- or B-cell tolerance may be induced with prohibits the subsequent IgG response to A.BY cells, possibly by way of suppressor T cells which may act either on B cells directly or via helper T cells.

Animals↗
PubMed1976

Genetic regulation of the antibody response to H-2Db alloantigens in mice. II. Tolerance to non-H-2 determinants abolishes the antibody response to H-2Db in B10.A(5R) mice.

B10.A(5R) mice (H-2i5), immunized with spleen cells from congenic B10 mice (H-2b), responded to alloantigens of the H-2Db region by producing antibodies of only IgM type. In contrast, they produced both IgM and IgG antibodies when immunized with noncongenic H-2b cells that carry other foreign cell surface antigens (non-H-2) in addition to H-2Db. A hypothesis was proposed comparing the H-2Db antigen on a congenic cell to a hapten on a nonimmunogenic carrier which fails to induce T-cell helper function responsible for the switch from IgM to IgG secretion in B cells. Data presented here confirmed this hypothesis. 5R mice rendered tolerant to the relevant non-H-2 antigens were unable to mount the anti-H-2Db IgG response in a noncongenic immunization. Tolerance induction did not lead to abrogation of the T-cell mediated cytotoxicity.

Animals↗
PubMed1975

Genetic regulation of the antibody response to H-2Db alloantigens in mice. I. Differences in activation of helper T cells in C57BL/10 and BALB/c congenic strains.

B10.A(5R) mice immunized with C57BL/10 spleen cells demonstrate a normal T-cell-mediated cytotoxicity to H-2Db tumor cells but they do not mount any IgG antibody response to H-2Db alloantigens. B10.A(5R) mice do show a high titered IgG response when immunized with A.BY cells, which differ at H-2Db plus non-H-2 cell surface antigens, or with B10.A(2R) cells, which differ at H-2Db, H-2Kk, and H-2Ik cell surface antigens. These findings indicate a failure of the T-helper cells to induce the switch from IgM to IgG when the H-2Db alloantigens are the only difference on the immunizing cell. In immunizing H-2d mice with congenic H-g2 cells which differ only in the H-2Db region, mice of the C57BL/10 background made only IgM antibodies whereas mice of the BALB/c background made IgG antibodies. This comparison confirms that genes separate from H-2 regulate the T-cell helper function. The genes that influence the T-cell helper function do not regulate the T-cell-mediated cytotoxicity.

Animals↗