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"The strict rules that normally govern T-cell activation are relaxed so that the host animal has the best possible chance of a maximal response and ultimately staying alive," says Stephen McSorley. (Credit: NIAID/NIH/Wikimedia Commons)

immune systems ,

T-cells break the rules when salmonella attacks

The immune system’s T-cells respond differently when the body is attacked by fast-acting bacteria, such as salmonella.

The finding could be vital for designing vaccines and medicines to prevent or treat deadly infectious diseases.

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“Our study shows that the body’s immune system functions very differently when it faces a rapidly growing pathogen like salmonella or chlamydia,” says immunologist Stephen McSorley, an associate professor at the Center for Comparative Medicine at the University of California, Davis.

“The strict rules that normally govern T-cell activation are relaxed so that the host animal has the best possible chance of a maximal response and ultimately staying alive,” he says.

T-cells, which belong to a group of white blood cells called lymphocytes, normally respond defensively to the presence of substances known as antigens, which are produced by invading bacteria and viruses. It’s widely known that T-cells launch an immune defense when they recognize specific antigens.

However in this study, the researchers demonstrated in the mouse that certain T-cells don’t require the presence of specific antigens to launch an effective immune response. During fast-moving salmonella and chlamydia infections, a cascade of other antimicrobial interactions occur that trigger these T-cells to respond defensively to the bacterial attacks, even without the presence of specific antigens.

The researchers also showed that when this defensive pathway was disrupted during salmonella infection, the mice had greater difficulty getting rid of the bacterial disease.

The researchers note that further study is needed to determine if this newly defined antimicrobial pathway also can provide protection against co-infections by multiple disease-causing microbes.

Additional researchers from UC Davis and Stanford University contributed to the study, which was published online in the journal Immunity.

The National Institutes of Health and the Vietnam Education Foundation provided funding for the project.

Source: UC Davis

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