Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UNIPROT:P30536 (
PBS
)
9,886
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Major histocompatibility complex class I-deficient islets from
beta-2 microglobulin
-deficient mice have been shown to have prolonged in vivo islet allograft survival. Additionally in vitro studies using the mixed lymphocyte islet coculture system have demonstrated a reduction in cytotoxic T lymphocyte activity against alloislets that have been pretreated with an antibody directed against MHC class I antigen. The clinical applicability of these findings are examined in this study, which evaluates the ability of MHC class I blocking antibody to prevent the in vivo destruction of alloislets. Recipients of allogenic islet transplants treated with phosphate-buffered saline or control F(ab')2 fragments rejected the transplanted alloislets in median times of 11.5 days and 11 days, respectively. Recipient mice treated with a monoclonal antibody or F(ab')2 fragments specific to the donor MHC class I antigen had significant prolongation in allograft survival (median allograft survival for both groups was 21 days) when compared with mice treated with
PBS
or control F(ab')2 fragment. These results demonstrate that treating recipients of alloislets with donor-specific MHC class I monoclonal antibody or the respective F(ab')2 fragments prolongs islet allograft survival. This confirms the importance of MHC class I antigen in the rejection of pancreatic islet allografts and suggests that blocking different domains on the MHC class I molecule could be used therapeutically in the protection of allografts from the immune system.
...
PMID:Prolongation of in vivo mouse islet allograft survival by modulation of MHC class I antigen. 815 21
Adult T-cell leukemia (ATL) consists of an overabundance of T cells, which express CD25. Therapeutic efficacy of astatine-211 ((211)At)-labeled murine monoclonal antibody 7G7/B6 alone and in combination with daclizumab was evaluated in nonobese diabetic/severe combined immunodeficiency (NOD/SCID) mice given injections of MET-1 human T-cell leukemia cells. Daclizumab and 7G7/B6 are directed toward different epitopes of CD25. Either a single dose of 12 microCi (0.444 MBq) (211)At-7G7/B6 per mouse given intravenously or receptor-saturating doses of daclizumab given at 100 microg weekly for 4 weeks intravenously inhibited tumor growth as monitored by serum levels of human
beta-2 microglobulin
(beta(2)mu) and by prolonged survival of leukemia-bearing mice compared with the control groups (P < .001). The combination of 2 agents enhanced the antitumor effect when compared with groups treated with 12 microCi (0.444 MBq) of (211)At-7G7/B6 (P < .05) or daclizumab alone (P < .05). The median survival duration of the
PBS
group was 62.6 days and 61.5 days in the radiolabeled nonspecific antibody (211)At-11F11-treated group. In contrast, 91% of mice in the combination group survived through day 94. These results that demonstrate a significantly improved therapeutic efficacy by combining (211)At-7G7/B6 with daclizumab support a clinical trial of this regimen in patients with ATL.
...
PMID:Effective treatment of a murine model of adult T-cell leukemia using 211At-7G7/B6 and its combination with unmodified anti-Tac (daclizumab) directed toward CD25. 1656 69