Amanda Ardain et al demonstrated an early protective role for innate lymphoid cells (ILCs) in immunity to Mycobacterium tuberculosis (Mtb) infection. Researchers found that among people who were infected with Mtb, a subset of ILCs moved from the blood to the lungs, where TB infections frequently take hold. The circulating subsets of ILCs which were depleted from the blood of participants with pulmonary TB was restored upon treatment. Tuberculosis increased accumulation of ILC subsets in the human lung, corresponding to a robust transcriptional response to infection. Investigators also tracked the activity of ILCs in mice models where group 3 ILCs (ILC3s) accumulated rapidly in Mtb-infected lungs which coincided with the accumulation of alveolar macrophages. Mice that lacked ILC3s exhibited a reduction in the accumulation of early alveolar macrophages and decreased Mtb control. The researchers showed that the C-X-C motif chemokine receptor 5 (CXCR5)–C-X-C motif chemokine ligand 13 (CXCL13) axis is involved in Mtb control. Interleukin-23-dependent expansion of ILC3s in mice and production of interleukin-17 and interleukin-22 were found to be critical inducers of lung CXCL13, promoting early innate immunity and the formation of protective lymphoid follicles within granulomas. The researchers suggest boosting this response may provide a new approach to developing treatments and vaccines against TB.
Source: Nature 5 June,2019 https://www.nature.com/articles/s41586-019-1276-2