Autoantibody potential of cancer therapeutic monoclonal antibodies.

We and others have reported that multiple autoantibodies are unmasked in human polyclonal antibody preparations after exposure to physiological oxidizing agents (hemin) or electromotive force. We now have asked if oxidation unmasks autoantibody reactivities in monoclonal antibodies (mAb). To do this, we have studied 9 FDA approved mAb used therapeutically, including 4 chimeric, 4 humanized and 1 chemically modified chimeric Fab that were exposed to the physiological oxidizing agent hemin at 36 degrees C for 20 hr.

Redox-reactive antiphospholipid antibody differences between serum from Alzheimer's patients and age-matched controls.

There is no universally acceptable inclusive laboratory biomarker for the diagnosis and staging of neurodegenerative diseases, for example, Alzheimer's. There is an abnormal increase of oxidative stress in the central nervous system (CNS) of Alzheimer's patients that causes oxidation of proteins, lipids and DNA. We have published that the antiphospholipid (aPL) autoantibodies that are members of the redox-reactive autoantibody (R-RAA) family, are significantly decreased or absent in the cerebrospinal fluids of autopsy-confirmed Alzheimer's disease (AD) patients.

Redox-reactive autoantibodies: biochemistry, characterization, and specificities.

Oxidation-reduction (redox) reactions can "unmask" autoantibody activity in blood and other body fluids from normal, healthy individuals. These "unmasked" autoantibodies are similar if not identical to autoantibodies associated with autoimmune diseases. The agents responsible for this unmasking are physiological oxidants such as hemin and likely other naturally occurring molecules in the body that contain transitional metals available for participation in redox reactions.

Redox-reactive autoantibodies in Alzheimer's patients' cerebrospinal fluids: preliminary studies.

Oxidation of cerebrospinal fluid (CSF) causes differential unmasking of autoantibodies in control CSF vs. that obtained from postmortem CSF samples from autopsy confirmed Alzheimer's disease (AD) cases. This study demonstrates that normal CSF from both living patients and from non-demented autopsy cases contains redox-reactive autoantibodies with specificities that include antiphospholipid antibodies (aPL).

Redox-reactive autoantibodies: detection and physiological relevance.

We recently described a hitherto unrecognized family of autoantibodies that become unmasked (detectable) subsequent to oxidation-reduction (redox) reactions. These masked redox-reactive autoantibodies are not detectable by using conventional immunoassays. Additional experimentation has demonstrated that autoantibodies in the blood of patients with autoimmune diseases can be masked (become undetectable) by exposure to oxidizing agents.

The appearance and disappearance of antiphospholipid autoantibodies subsequent to oxidation--reduction reactions.

The mechanisms that cause the appearance of autoantibodies are not understood. Compared to normal antibody production, factors responsible for autoantibody synthesis are more complex; they are thought to disrupt the normal mechanisms proposed to eliminate or down-regulate self-antibodies or to interfere with anti-self-receptor editing. Data presented show that autoantibodies exist in the blood of all normal individuals.

Woundoscopy: a new technique for examining deep, nonhealing wounds.

This article discusses a standard gastrointestinal procedure used to visualize sinus tracts in wounds. Sinus tracts have traditionally been visualized externally and probed internally. Because of this, the cause of the nonhealing wound was difficult to determine.