Recent allergy research has focused on a family of cells in the immune system proven to play a critical role in allergic responses.
Known as innate lymphoid cells, or ILCs, they can kill or regulate various cell types to fight pathogens and protect against infections – but at the same time may exacerbate allergies by over-responding and causing inflammation.
Now, researchers have discovered a protein in the bone marrow that drives production of these influential immune cells, according to findings led by the Mary H. Weiser Food Allergy Center at Michigan Medicine that appears in Science Immunology.
“We have identified a regulatory molecule that controls the production of cells that are critical to mediating allergic responses,” says lead author Chang Kim, Ph.D., Michigan Medicine pathologist and researcher with the allergy center.
“A better understanding of how these cells are made and regulated brings us closer to a novel target to treat inflammatory and allergic diseases through new therapies in the future.”
Researchers found that this protein (BATF) regulates the gene expression required for the differentiation of the ILCs immune cells in the bone marrow.
ILCs are counterparts to T-cells that contribute to immune responses. In addition to their role in allergy responses, ILCs protect from diverse pathogens such as bacteria, viruses, and parasites like tapeworms. They also help regulate fat mass, metabolism, and microbiome.
The study found that animals deficient in the expression of BATF are highly susceptible to infection and are unable to mount an effective immune response to allergy-inducing cytokines.
“Animals deficient in this molecule are protected from allergic responses,” Kim says. “This tells us that our research may provide useful information regarding mechanisms of allergic immune responses.”
Kim’s lab continues research on the molecular details in the regulation of ILC production that may lead to novel targets of intervention.
Study cited: “BATF regulates innate lymphoid cell hematopoiesis and homeostasis,” Science Immunology, DOI: 10.1126/sciimmunol.aaz8154
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