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At least 883 records · Page 49Linked to original sources
PubMed1996

Bispecific antibody-mediated immunotherapy of the BCL1 lymphoma: increased efficacy with multiple injections and CD28-induced costimulation.

The BCL1 lymphoma in Balb/c mice can be successfully treated with bispecific (anti-CD3 x anti-idiotype) antibodies (BSABs). In these experiments, animals were injected intraperitoneally (IP) with 5 x 10(3) tumor cells (day 0) and treated with one single intravenous (IV) injection of 5 micrograms BSAB (day 9). Because cross-linking of the CD3 complex is not in itself sufficient to activate resting T cells, the therapeutic success was mainly based on the progressive retargeting of the relatively small cytotoxic T-lymphocyte effector cell pool already in existence in vivo. For this reason, the therapy lost its effectiveness at higher tumor loads. Two possibilities were explored to treat mice with a higher tumor load (10(5) tumor cells). First multiple injections of BSABs were used, but a dose-related monovalent anti-CD3 immunosuppression was induced. This approach was only beneficial when the immune system was able to recover from the previous injection of BSAB. As a second approach, CD28 costimulation together with BSABs were used in an attempt to activate resting T cells, ultimately enlarging the effector T-cell pool. However, we were repeatedly unsuccessful in attempts to improve our in vivo results using young, naive animals in which the majority of T cells are of the naive phenotype. Only when animals were primed to induce the memory T-cell type was a significantly better outcome observed, and then only with multiple injections of BSABs and anti-CD28 monoclonal antibodies (MoAbs), rather than with BSAB or anti-CD28 MoAb alone. These results suggest that this combination was able to activate memory and effector T cells and to focus them on the tumor, but was unable to activate naive T cells fully. The in vivo potency of the BSAB and CD28 costimulation was shown by the fact that one-tenth of the quantity of BSAB was required to cure animals with 20 times the tumor load.

Animals↗
PubMed1995

Monitoring of allograft recipients for the development of HLA-specific antibodies: elimination of OKT3 as a complicating factor.

In this report we demonstrate that the use of immunoabsorbent beads to remove the OKT3 monoclonal antibody (MoAb) from the sera of transplant recipients is necessary in order to avoid the false positive reactivity in panel reactive antibody (PRA) assay. We have shown that the presence of OKT3 MoAb in patient's sera can give a positive reactivity in PRA, which may be interpreted as antibody development. Rabbit antimouse immunoglobulin covalently linked to sepharose can effectively remove the OKT3 MoAb from patients sera, but has no effect on anti-HLA antibodies. The absorbance of OKT3 MoAb, therefore, is necessary to obtain accurate results in respect to humoral rejection, which may lead to mismanagement of patients.

Antibody Formation↗
PubMed1995

Immunologic monitoring of OKT3 induction therapy in cardiac allograft recipients.

OKT3 induction therapy was monitored in 31 cardiac allograft recipients during the 1st year posttransplant. Serum level of OKT3, anti-OKT3 antibodies, and interleukin-2 (IL-2) were monitored during the first 2 months posttransplant. These values were retrospectively correlated with allograft rejection episodes which occurred during the 1st year posttransplant and allograft survival rates over a 3-year observation period. We found that OKT3 induction therapy (10-14 days) was not associated with the development of anti-OKT3 antibodies manifest by dropping OKT3 levels during OKT3 therapy, and is not associated with the development of vascular rejection in our patient population. Patients with high titer ant-OKT3 antibodies, erratic serum OKT3 levels, and/or high serum IL-2 levels (> or = 5 ng/ml) during the first 2 months posttransplant showed a higher incidence of allograft rejection (predominantly cellular rejection) during the 1st year posttransplant and showed lower allograft survival rates. We also showed that a concomitant elevation of serum IL-2 levels was found in patients who developed anti-OKT3 antibodies. CD3+ T-cell levels were not predictive of inefficacy of OKT3 therapy. We conclude that immunologic monitoring of serum OKT3, anti-OKT3 antibody, and possibly serum IL-2 levels is critical for identification of patients who develop early, OKT3-resistant rejection episodes and for the identification of patients who may be more susceptible to allograft rejection and decreased allograft survival long after completion of OKT3 therapy.

Antibodies, Anti-Idiotypic↗