Researchers from Weill Cornell Medicine led a new study on group 2 innate lymphoid cells (ILC2s) and found that these cells have an important role in the immune system against parasitic infections, allergic inflammation, and asthma.
According to the press release, the study's findings answer the problem of the possible redundancy of ILC2s with other cells in the body. More so, the study suggests a unique set of regulatory networks that neurons control could be viable targets for future drug therapies to combat chronic inflammatory diseases, like inflammatory bowel disease (IBD), allergy, and asthma.
New Study Advances Understanding of Immune System Complexities Against Inflammation to Identify New Targets for Future Therapies
Group 2 innate lymphoid cell (ILC2) Explained
ILC2 is a recently discovered family of white blood cells found in the skin, gastrointestinal tract, airways, and other barriers of tissues in the body. This cell is part of the family of cells that were discovered by multiple groups 12 years ago.
Researchers found that ILC2 serves as sentinels and first responders against infection, and may hold the key to understanding common inflammatory and autoimmune conditions, like asthma and IBD.
According to a 2012 paper published in the Annual Review of Immunology, ILCs are immune cells that lack specific antigen receptors but can still produce an array of effector cytokines that match T helper cell subsets.
Moreover, these cells function in lymphoid organogenesis, tissue remodeling, antimicrobial immunity, and inflammation in barrier surfaces of tissues. They promptly work to respond against stress-causing microbes, making them effective first-line immunological defenses.
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ILC2 vs. T Helper Cells
The study, titled "Neuropeptide regulation of non-redundant ILC2 responses at barrier surfaces" published in Nature, discussed how ILC2s differ from T helper type 2 cells (Th2 cells). Researchers determined that the latter cannot adequately compensate for the loss of the protective response of ILC2 against gut inflammation, and parasitic worm infection.
Dr. David Artis, the study's senior author, said in the press release that the findings of the study advance the understanding of the complexities of the immune system and gives insights into a potential new set of targets for future therapies.
ILC2 and Th2 are thought to have evolved in part to defend the body against parasitic worm infections. So when triggered, they both help a type 2 immune response.
Researchers suggest that both cells are functionally the same, although ILC2 specializes in earlier and more localized responses, while Th2 cells are more blood-borne and mobile that concentrates in multiple tissues where it is needed. But they also found that ILC2 has a more essential role than just being redundant as type 2 immune responders.
The team found in their experiments on mice models that those mice with deleted ILC2 have become more susceptible to parasitic worm infection in the gut, and gut damage from inflammation because of reduced capacity to produce an anti-parasitic immune response compared to mice with normal ILC2s.
The findings suggest that neurons in the gut communicate with ILC2s to produce an immune response that cannot be replicated by any other immune cells. Clarifying the role of ILC2s is a significant achievement in basic immunology that may lead to new targets for future therapeutics.
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