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Antibody can block B cells from fighting pathogens among HIV patients

By Allen Cone
This is a colorized scanning electron micrograph of a B cell from a human donor. Researchers found a type of antibody can stop the immune system's B cells from fighting pathogens in HIV infections. Image courtesy of National Institute of Allergy and Infectious Diseases
This is a colorized scanning electron micrograph of a B cell from a human donor. Researchers found a type of antibody can stop the immune system's B cells from fighting pathogens in HIV infections. Image courtesy of National Institute of Allergy and Infectious Diseases

Aug. 13 (UPI) -- A type of antibody can stop the immune system's B cells from fighting pathogens in HIV infections, according to research.

Scientists at the National Institute of Allergy and Infectious Diseases found the antibody, called immunoglobulin G3, or IgG3, prevents the B cells from operating normally. The researchers, from the National Institutes of Health, published their findings Monday in the journal Nature Immunology.

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B cells produce antibodies that are used to attack invading bacteria, viruses, and toxins. And T cells -- specially called CD4 -- destroy the body's own cells that have been taken over by viruses or become cancerous.

In HIV, which stands for the human immunodeficiency virus, the immune system becomes weakened because the infected cells die.

Although the antibody appears to be one way for the body to reduce the potentially damaging effects of immune-system hyperactivity in HIV, it also impairs normal immune function, researchers noted in an NIH press release.

The investigators analyzed blood samples from 83 HIV-uninfected, anonymous donors and 108 people with HIV at various stages of infection. Some were being treated for their infection.

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IgG3 appeared on the surface of B cells only under certain conditions -- mainly people living with HIV but not in HIV-uninfected people.

In addition, IgG3 predominantly appeared on B cells of African Americans or black African decent during the chronic phase of untreated HIV infection when it was not adequately controlled.

B-cell receptor normally bind to foreign entities such as pathogens, stimulating them to produce many copies of the antibody form of the receptor. This can trap a pathogen and mark it for destruction.

But among people living with HIV, the IgG3 short-circuits this process by docking on the B-cell receptor and blocking it from adequately responding to the pathogen or other intended target.

In addition, other components of the immune system contribute to IgG3 interference with normal B-cell function during HIV infection.

When a chronically infected person starts treatment to control the virus, the IgG3 stops binding to B-cell receptors.

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