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Abstract
The discovery of innate lymphoid cells (ILCs) has revolutionized our understanding of innate immunity and immune cell interactions at epithelial barrier sites. Their presence and maintenance are critical for modulating immune homeostasis, responding to injury or infection, and repairing damaged tissues. To date, ILCs have been defined by a set of transcription factors, surface antigens and cytokines, and their functions resemble those of three major classes of helper T cell subsets, Th1, Th2 and Th17. Despite this, the lack of antigen-specific surface receptors and the notion that ILCs can develop in the absence of the thymic niche have clearly set them apart from the T-cell lineage and promulgated a dogma that ILCs develop directly from progenitors in the bone marrow. Interestingly however, emerging studies have challenged the BM-centric view of adult ILC development and suggest that ILCs could arise neonatally from developing T cell progenitors. In this review, we discuss ILC development in parallel to T-cell development and summarize key findings that support a T-cell-centric view of ILC ontogeny.
Highlights
While hints of innate type immune cell subsets, including NK cells and lymphoid tissue inducer (LTi) cells, were discovered as early as 1970s and early 2000s respectively [1, 2], a more detailed and full characterization of the innate lymphoid cell (ILC) family emerged in the late 2000s [3]
Through elegant pulse-labeling of putative BM and fetal ILC precursors (Id2+ and Arg-1+ respectively) [30, 62], this group showed that development of ILC2s is temporally controlled and that they follow the model of layered lymphopoiesis similar to the one described in early macrophage development. These findings argue that ILC2s rapidly colonize peripheral tissues during the first week or two of postnatal life in mice and at a time when the bone marrow (BM) is still establishing itself as the sole source of hematopoietic progenitor activity
In our previous studies of murine ILC2 genomic loci and transcripts, we found that the rearranged loci are transcriptionally silent in murine ILC2s as well, potentially reflecting an attempt to silence alleles that have failed productive in-frame rearrangement; a process that naturally occurs in developing thymocytes
Summary
While hints of innate type immune cell subsets, including NK cells and lymphoid tissue inducer (LTi) cells, were discovered as early as 1970s and early 2000s respectively [1, 2], a more detailed and full characterization of the innate lymphoid cell (ILC) family emerged in the late 2000s [3]. These studies found that ILCs do not undergo TCR-dependent development or activation, the factors required for their commitment and maturation are virtually indistinguishable from those found in T-cell development with the noteworthy exception of NFIL3 expression in early BM ILC progenitors [18, 32,33,34].
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