PubMed Health⌕ Search

PubMed · 15896765

Use of rituximab to decrease panel-reactive antibodies.

Abstract

Patients with pre-formed antibodies may be at increased risk of rejection after organ transplantation. In this report, we describe the use of rituximab to decrease the percentage of pre-formed antibodies in a pediatric heart transplant recipient.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Ian C Balfour, Andrew Fiore, Ralph J Graff, Alan P Knutsen. 2005. Use of rituximab to decrease panel-reactive antibodies.. https://doi.org/10.1016/j.healun.2004.01.006

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

ERBB3 overexpression due to miR-205 inactivation confers sensitivity to FGF, metabolic activation, and liability to ERBB3 targeting in glioblastoma.

In glioblastoma (GBM), the most frequent and lethal brain tumor, therapies suppressing recurrently altered signaling pathways failed to extend survival. However, in patient subsets, specific genetic lesions can confer sensitivity to targeted agents. By exploiting an integrated model based on patient-derived stem-like cells, faithfully recapitulating the original GBMs in vitro and in vivo, here, we identify a human GBM subset (∼9% of all GBMs) characterized by ERBB3 overexpression and nuclear accumulation. ERBB3 overexpression is driven by inheritable promoter methylation or post-transcriptional silencing of the oncosuppressor miR-205 and sustains the malignant phenotype. Overexpressed ERBB3 behaves as a specific signaling platform for fibroblast growth factor receptor (FGFR), driving PI3K/AKT/mTOR pathway hyperactivation, and overall metabolic upregulation. As a result, ERBB3 inhibition by specific antibodies is lethal for GBM stem-like cells and xenotransplants. These findings highlight a subset of patients eligible for ERBB3-targeted therapy.

Antibodies↗

MUC1 is a scaffold for selectin ligands in the human uterus.

MUC1 is a large, transmembrane mucin glycoprotein abundantly expressed at the apical surface of uterine epithelia in all species examined to date. Loss of MUC1 at the time of embryo implantation occurs in many species; however, this does not appear to be the case in humans. Recent studies indicate that human blastocysts express L-selectin at their external surfaces raising the possibility that selectin ligands expressed at the apical surface of the uterine epithelium support early stages of blastocyst attachment. In the current study, we have used a panel of antibodies specific for selectin ligands to determine if MUC1 functions as a scaffold for these carbohydrate motifs in fertile women. The results demonstrate that MUC1 carries selectin ligands throughout the secretory phase of the menstrual cycle, including the mid-secretory (receptive) phase. Consequently, MUC1 represents a potential ligand for selectins expressed by human blastocysts.

Antibodies↗

Patients with quinine-induced immune thrombocytopenia have both "drug-dependent" and "drug-specific" antibodies.

Immune thrombocytopenia induced by quinine and many other drugs is caused by antibodies that bind to platelet membrane glycoproteins (GPs) only when the sensitizing drug is present in soluble form. In this disorder, drug promotes antibody binding to its target without linking covalently to either of the reacting macro-molecules by a mechanism that has not yet been defined. How drug provides the stimulus for production of such antibodies is also unknown. We studied 7 patients who experienced severe thrombocytopenia after ingestion of quinine. As expected, drug-dependent, platelet-reactive antibodies specific for GPIIb/IIIa or GPIb/IX were identified in each case. Unexpectedly, each of 6 patients with GPIIb/IIIa-specific antibodies was found to have a second antibody specific for drug alone that was not platelet reactive. Despite recognizing different targets, the 2 types of antibody were identical in requiring quinine or desmethoxy-quinine (cinchonidine) for reactivity and in failing to react with other structural analogues of quinine. On the basis of these findings and previous observations, a model is proposed to explain drug-dependent binding of antibodies to cellular targets. In addition to having implications for pathogenesis, drug-specific antibodies may provide a surrogate measure of drug sensitivity in patients with drug-induced immune cytopenia.

Antibodies↗