Human and murine anti-Rh monoclonal antibodies. A comparison of serological, immunochemical, cellular and functional activity

Kumpel, Belinda M.; Leader, K A; Poole, Geoff; Yendle, Janet; Judson, P. A.

doi:10.1016/s0338-4535(88)80104-1

Cited by 6 publications

(2 citation statements)

References 12 publications

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“…In tests against selected MAb-D (12 IgM and 31 IgG) a similar pattern of reactions, different from those of the D category, DFR and R 0 Har phenotypes (Table 2), was observed with cells of seven of the eight probands. Proband 1 was tested by two laboratories for the ISBT monoclonal workshop in Paris in 1987 (Kumpel et al, 1988;Tippett & Lomas, 1988); a more recent sample was not available and therefore fewer MAb-D have been tested but sufficient tests were done to show that proband 1 probably has the same partial D antigen. Variable reactions occurred with some MAb-D: cells of proband 4 appeared to have stronger expression and cells of probands 5 and 8 to have weaker expression of the partial D antigen than that of the other probands.…”

Section: Reactions With Monoclonal Anti-dmentioning

confidence: 99%

DBT: a partial D phenotype associated with the low‐incidence antigen Rh32

Wallace

Lomas‐Francis

Beckers

et al. 1997

Transfusion Medicine

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Eight probands are described with a D phenotype in which a partial D antigen is associated with Rh32 antigen; three of these probands were investigated because of the anti-D in their serum. The partial D lacks epD1-epD5 and epD9 and some epD6/7 and only expresses epD8 and other parts of epD6/7. The strength of the partial D antigen varies between unrelated DBT individuals. The Rh32 antigen of the DBT cells is weaker than that of D(C)(e) cells. Tests on DBT, DFR and R0Har cells with anti-epD6/7 split these monoclonal anti-D into eight patterns of reaction. A new pattern of reactions was observed, presaging a new epitope, but this was not numbered.

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Section: Reactions With Monoclonal Anti-dmentioning

confidence: 99%

DBT: a partial D phenotype associated with the low‐incidence antigen Rh32

Wallace

Lomas‐Francis

Beckers

et al. 1997

Transfusion Medicine

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“…As the availability of RhIg donors is limited and the only available immunoprophylaxis is against RhD, there is a critical need to develop monoclonal antibody alternatives to RhIg and immunoprophylaxis to other RBC antigens. As different monoclonal antibodies to the RhD antigen can have differential immunological outcomes, understanding the mechanism regarding how monoclonal antibodies induce AMIS can facilitate the development and accurate assessment of monoclonal antibodies against RhD and other RBC antigens.…”

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confidence: 99%

Antibody‐mediated immunosuppression can result from RBC antigen loss independent of Fcγ receptors in mice

et al. 2018

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BACKGROUND: Anti-RhD administration can prevent de novo anti-RhD formation following RhD+ red blood cell (RBC) exposure, termed antibody-mediated immunosuppression (AMIS). Recent studies suggest that AMIS may occur through target antigen alterations, known as antigen modulation. However, studies suggest that AMIS may occur independent of antigen modulation. In particular, AMIS to RBCs that transgenically express the fusion hen egg lysozyme-ovalbumin-Duffy (HOD) antigen have been shown to occur independent of activating Fcγ receptors (FcγRs) thought to be required for antigen modulation. Therefore, we sought to determine the mechanism behind AMIS following HOD RBC exposure. STUDY DESIGN AND METHODS: Following transferof HOD RBCs into wild-type or FcγR-chain knockout recipients in the presence or absence of monoclonal anti-hen egg lysozyme (HEL) antibody, individually or in combination, HOD antigen levels and anti-HOD antibody formation were examined.ABBREVIATIONS: AMIS = antibody-mediated immunosuppression; DAT = direct antiglobulin test; FcγRs = Fcγ receptors; HEL = hen egg lysozyme; HOD = hen egg lysozymeovalbumin-Duffy; mHEL = membrane-bound form of HEL.

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Heterogeneity in the ability of IgG1 monoclonal anti‐D to promote lymphocyte‐mediated red cell lysis

et al. 1989

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Thirty-four IgG anti-D human monoclonal antibodies (mAb) derived from 18 donor were assessed for their ability to mediate lysis of D+ red cells by lymphocytes in antibody-dependent cell-mediated cytotoxicity assays. Cell-bound antibody was quantified and the mAb were compared at similar levels of sensitization. The majority (23/31) of IgG1 and all (3/3) IgG3 mAb were ineffective; two donors produced both lytic and non-lytic anti-D mAb. Greater sensitivity was achieved using fluid-phase antibody (as culture supernatants) in the assay than was obtained with pre-sensitized red cells. Minimum levels of 2000 anti-D molecules per cell were required for lysis using pre-sensitized cells. Partial D red cells (DIVa, DVa and DVI) were lysed by three mAb that were lytic with normal D+ cells. There was no relationship between lytic ability and Gm allotype or D epitope specificity of the antibodies. Four mAb to other blood group specificities were tested: two (anti-E and anti-G) were lytic and two (anti-c and anti-Kell) were not lytic. Possible reasons for the heterogeneity of the lytic activity by the mAb are discussed.

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Human and murine anti-Rh monoclonal antibodies. A comparison of serological, immunochemical, cellular and functional activity

Cited by 6 publications

References 12 publications

DBT: a partial D phenotype associated with the low‐incidence antigen Rh32

DBT: a partial D phenotype associated with the low‐incidence antigen Rh32

Antibody‐mediated immunosuppression can result from RBC antigen loss independent of Fcγ receptors in mice

Heterogeneity in the ability of IgG1 monoclonal anti‐D to promote lymphocyte‐mediated red cell lysis

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