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1 ntigen system was established by analysis of lymphocytotoxic alloantibodies that were made by pregnan
2 ted the hypothesis that replacement of their lymphocytotoxic and nephrotoxic immunosuppression (combi
3  at the time of the biopsy were screened for lymphocytotoxic anti-HLA antibodies.
4                        Presence of preformed lymphocytotoxic antibodies may represent a barrier to is
5                              The presence of lymphocytotoxic antibody (LCTAB) correlates well with re
6 r coagulation, increasing height and weight, lymphocytotoxic antibody positivity, an increasing numbe
7  Platelet refractoriness was associated with lymphocytotoxic antibody positivity, heparin administrat
8         The PG27/CsA combination blocked the lymphocytotoxic antibody response and IgG and IgM xenoan
9            CsA suppressed the heterospecific lymphocytotoxic antibody response and inhibited IgG but
10 ve historical and pretransplant standard NIH lymphocytotoxic cross-matches and received the same immu
11 r allografts transplanted against a positive lymphocytotoxic crossmatch (CDC+) are susceptible to an
12           All underwent complement-dependent lymphocytotoxic crossmatch (CDC-XM) with pre- and posttr
13 A+ liver allograft recipients as measured by lymphocytotoxic crossmatch (XM) and/or Luminex.
14 ow cytometric crossmatch FCXM+, and positive lymphocytotoxic crossmatch CDC+.
15  activity reported with a single course of a lymphocytotoxic drug in patients with mainly relapsed an
16        Fifty-three patients who received the lymphocytotoxic mAb CAMPATH-1H between 1991 and 1994 in
17 data are also relevant to patients receiving lymphocytotoxic mAb therapy for other indications, and t
18 studied patients who had previously received lymphocytotoxic monoclonal antibody (mAb) therapy for rh
19  in 53 RA patients who were treated with the lymphocytotoxic monoclonal antibody alemtuzumab between
20  clinicians and patients who are considering lymphocytotoxic or other immunomodulatory therapy for RA
21 uzumab might be active in SAA because of its lymphocytotoxic properties.
22 *51011 amino acid mismatches, explaining the lymphocytotoxic reactivity pattern.
23   The PRA screen was performed by use of the lymphocytotoxic technique treated with dithiothreitol to
24 correlate with the lymphocyte count prior to lymphocytotoxic therapy; however, after therapy the degr

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