Abstract
Lower respiratory infections are among the leading causes of morbidity and mortality worldwide. These potentially deadly infections are further exacerbated due to the growing incidence of antimicrobial resistance. To combat these infections there is a need to better understand immune mechanisms that promote microbial clearance. This need in the context of lung infections has been further heightened with the emergence of SARS-CoV-2. Group 3 innate lymphoid cells (ILC3s) are a recently discovered tissue resident innate immune cell found at mucosal sites that respond rapidly in the event of an infection. ILC3s have clear roles in regulating mucosal immunity and tissue homeostasis in the intestine, though the immunological functions in lungs remain unclear. It has been demonstrated in both viral and bacterial pneumonia that stimulated ILC3s secrete the cytokines IL-17 and IL-22 to promote both microbial clearance as well as tissue repair. In this review, we will evaluate regulation of ILC3s during inflammation and discuss recent studies that examine ILC3 function in the context of both bacterial and viral pulmonary infections.
Highlights
Th1 and Th2 helper cell subsets were initially defined by cytokine secretion [1, 2] and this was expanded to other T cell subsets including Th17 cells in the early 2000s, which demonstrated that IL-17 secreting CD4+ T cells arise independent of transcription factors of Th1 (STAT4) and Th2 (STAT6) cells [3,4,5]
Ex vivo stimulation of ILC3s isolated from K. pneumoniae infected mice with inducible T cell costimulatory molecule (ICOS) ligand (ICOSL) resulted in proliferation of cells [33], indicating the ICOS : ICOSL pathway may be important in mediating ILC3 function and proliferation (Figure 1)
As ILC3s are maintained in lung tissue and can rapidly produce IL-17 and IL-22 upon stimulation, it is clear that they play an important role in the innate immune response against bacterial pneumonia [45]
Summary
Th1 and Th2 helper cell subsets were initially defined by cytokine secretion [1, 2] and this was expanded to other T cell subsets including Th17 cells in the early 2000s, which demonstrated that IL-17 secreting CD4+ T cells arise independent of transcription factors of Th1 (STAT4) and Th2 (STAT6) cells [3,4,5]. These cytokines function to enhance production of antimicrobial proteins, facilitate barrier repair through promotion of epithelial cell proliferation, and augment neutrophil recruitment, resulting in increased clearance of pulmonary pathogens [28,29,30]. Ex vivo stimulation of ILC3s isolated from K. pneumoniae infected mice with ICOS ligand (ICOSL) resulted in proliferation of cells [33], indicating the ICOS : ICOSL pathway may be important in mediating ILC3 function and proliferation (Figure 1).
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