A study published in the journal Nature Immunology reveal a gene that is essential for embryo survival could also be the key to treating chronic infections such as HIV. Genes are the working subunits of DNA, where DNA stand for Deoxyribonucleic acid, a chemical information database that carries the complete set of instructions for the cell as to the nature of the proteins produced by it, its life span, maturity, function and death. Therefore, each gene contains a particular set of instructions, usually coding for a particular protein or for a particular function. The gene, called Arih2 produce a protein that is fundamental to the function of the immune system, making critical decisions about whether to switch on the immune response to an infection.
Researchers said that Arih2 is found in dendritic cells, the sentinels of the immune system that play an essential role in raising the alarm about the presence of foreign invaders in the body.
But while our immune system works well against many infections, chronic overwhelming infections such as HIV ‘exhaust’ and switch off the immune system, similar to autoimmune diseases such as rheumatoid arthritis and sepsis.
Indeed, during evolution, some organisms have evolved ways of exhausting our immune system to the point where the immune system just switches off, and this is what happens in HIV, hepatitis B, and tuberculosis. These organisms counter the immune response – exhausting T cells which are stimulated over and over again by the infection and becoming exhausted or paralyzed.
In the study, mice that were deficient in ARIH2 died before birth (embryonic lethal). Some of the mice with a mixed genetic background survived to birth but succumbed to an aggressive multi-organ inflammatory response.
Hence, the researchers are now looking at the effect on the immune response of switching off Arih2 for short periods of time during chronic infections.
This discovery has significant implications for manipulating the immune response to infections and suppressing chronic inflammation or autoimmunity because we can target this gene to try to push immune responses in one or other direction – either promoting it or suppressing it.
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