How viruses affect the immune system

Fighting infections depends on bodies' capacity to quickly recognize infected cells and destroy them, a job done by a class of immune cells known as CD8+ T cells. These soldiers get some of their orders from chemical mediators known as cytokines that make them more or less responsive to outside threats. In most cases, CD8+ T cells quickly recognize and destroy infected cells to prevent the infection from spreading.

When it comes to viruses that lead to chronic infection, immune cells receive the wrong set of marching orders, which makes them less responsive," says Martin Richer, an assistant professor at McGill's Department of Microbiology & Immunology and senior author of the study. The research, conducted in Richer's lab by graduate student Logan Smith, revealed that certain viruses persist by driving the production of a cytokine that leads to modification of glycoproteins on the surface of the CD8+ T cells, making the cells less functional.

That maneuver creates time for the pathogen to outpace the immune response and establish a chronic infection. Importantly, this pathway can be targeted to restore some functionality to the T cells and enhance the capacity to control infection. The discovery of this regulatory pathway could help identify new therapeutic targets for a variety of diseases.
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How obesity causes breast cancer

Obesity leads to the release of cytokines into the bloodstream which impact the metabolism of breast cancer cells, making them aggressive to treatment.
Severe overweight can lead to various health impairments. Besides inducing cardiovascular diseases, obesity for example also promotes the development of cancer and metastases.

ACC1 acetyl-CoA-carboxylase 1, a central component of fatty acid synthesis. ACC1 mediates the chemical addition of carbon dioxide to acetyl-CoA, which results in malonyl-CoA. This reaction is the first and speed determining step in the fatty acid synthesis of all living organisms.

ACC1 enzymes is a key component of fatty acid synthesis, its function is impaired by the cytokines leptin and TGF-β. The levels of these cytokines are increased particularly in the blood of severely overweight people.

Fatty acid precursors promote metastasis. The inhibition of ACC1 leads to the accumulation of the fatty acid precursor acetyl-CoA. This precursor is transferred to certain gene switches that in turn increase the metastatic capacity of cancer cells by activating a specific gene program.

Scientists used human tissue from breast cancer metastases to show that ACC1 was less active. When the scientists blocked the unknown signaling pathway with an antibody directed against the leptin receptor, this led to a significantly reduced metastatic spread of breast cancer tumors in an experimental model.
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Immune and nerve cells fight gut infections

Nerve cells in the gut play a crucial role in the body's ability to produce an immune response to infection. The immune system and nervous system worked together to respond to infectious threats.

The immune system and neuronal system don't act independently,
The lining of the gut house many immune system cells, which serve as a defense against parasites and other infections.

It is also loaded with nerve cells, immune system cells in the gut, called group 2 innate lymphoid cells (ILC2s), are intertwined with nerve cells called cholinergic neurons.

The ILC2 cells have a receptor for a protein called neuromedin U (NMU), which acts as a messenger for the nerve cells. Exposing ILC2 cells to NMU causes the ILC2 cells to multiply rapidly and secrete chemicals called cytokines that may help trigger an immune response or cause inflammation.

Administering NMU to mice infected with a gut parasite triggered inflammation and a powerful
immune response that expel the parasites quickly.

This shows that the NMU-producing nerve cells help the ILC2 cells, enabling them to rapidly and effectively respond to infection. The findings may improve fighting and provision of therapies for inflammatory diseases like asthma, food allergies and inflammatory bowel diseases.
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