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Helper T cells become polarized to effect a 'division of labor'. Sallusto and Spits and colleagues identify a new subset of skin-homing helper T cells, T_H-22 cells, that secrete interleukin 22.

Innate lymphoid cells are important players in the innate immune response, and might also contribute to inflammatory diseases. This Review discusses what is known about these cells and how they might be targeted in future therapies for these diseases.

Mice have lineage-negative IL-7Rα⁺ (innate lymphoid) cells that contribute to type 2 immunity. Spits and colleagues identify a similar CRTH2⁺CD161⁺ population in human lungs and gut that produces IL-13 after stimulation.

Innate lymphoid cells (ILCs) play critical immunological roles including immune surveillance at mucosal sites. Here the authors show that during nasal inflammation pathogen-induced cytokine production guides the differentiation of ILCs.

Recent studies have identified a new population of interleukin-22-producing cells in mucosal tissues that share features with both lymphoid-tissue inducer cells and natural killer cells. How are these three cell populations related and what might be the function of the new cell population?

Transdifferentiation between group 1 and group 3 innate lymphoid cells (ILCs) has been observed in the gut. Spits and colleagues now show lung ILC2s are able to convert into ILC1s in an IL-12-dependent manner.

Innate lymphoid cells are cytokine-producing cells that contribute to tissue homeostasis. Spits and colleagues identify a human innate cell population that expresses T-bet and IFN-γ and is prevalent in Crohn's disease.

Like T cells and B cells, innate lymphoid cells (ILCs) develop from common lymphoid progenitors, but how commitment to the ILC lineage is regulated has remained unclear. The transcriptional regulator TOX is important in this process.

Two humanized mouse models open up a plethora of research applications.

NK cells and ILC1s are developmentally distinct but share many functional similarities. Spits and colleagues describe current knowledge on the biology of these cells and the conditions under which they can be distinguished.

Innate lymphoid cells (ILCs) have key roles in immune responses, lymphoid tissue development and tissue regeneration. Recently, several new ILC subsets were identified. Here, the authors propose the use of a uniform nomenclature to describe all ILC subsets to avoid confusion and further promote the development of this field.

A family of innate lymphoid cells exist that is capable of rapid cytokine production. Spits and Di Santo review the developmental relationships and physiologic function of this expanding family.

Innate lymphoid cells (ILCs) can exhibit considerable plasticity. Humbles and colleagues identify a subpopulation of ILC2s in humans that can convert to proinflammatory ILC3s with implications for human skin diseases.

Type 2 innate lymphoid cells (ILC2s) are implicated in lung diseases such as idiopathic pulmonary fibrosis, but targeting these cells is a challenge. New data show that neuropilin-1 drives the ILC2 phenotype and is specific to lung-resident ILC2s in mice.

Respiratory pathogens and the human immune response they elicit can now be studied in humanized mice.

The importance of human innate lymphoid cells to normal human physiology is unclear. Vivier and colleagues find that immunodeficient patients ‘rescued’ with normal bone marrow can recover their T cells but not their innate lymphoid cells, yet remain entirely asymptomatic for nearly 40 years.

Phenotypic markers that overlap between ILC1 and NK populations have impacted the robust and specific analysis of these immune cell populations. Employing scRNA sequencing here the authors identify CD127⁺ CD94⁺ innate lymphoid cells that express granulysin and perforin and are expanded in patients with Crohn’s disease.

Murine ILCs can modulate T cell responses in MHCII-dependent manner. Here the authors show that human ILCs process and present antigens and induce T-cell responses upon exposure to IL-1-family cytokines; along with the article by Lehmann et al, this work elucidates how cytokines set context specificity of ILC-T cell crosstalk by regulating ILC antigen presentation.

Ton Schumacher and colleagues show that melanoma patients have CD4+ T cells reactive to mutated tumor antigens.

Emerging data suggest a lymphoid origin of plasmacytoid dendritic cells (pDCs), which, in most cases, do not share the classical functional properties of myeloid dendritic cells. This Comment proposes that pDCs should be assigned to a subcategory of innate lymphocytes and should be referred to as interferon-producing cells.

Mouse lymphoid tissue–inducer (LTi) cells require the transcription factor RORγt. Cupedo's group identifies RORγt⁺ human LTi cell equivalents as committed natural killer cell precursors, and teams led by Vivier and Diefenbach describe RORγt-expressing interleukin 22–producing natural killer cells in mouse gut.

Type 2 innate lymphoid cells (ILC2s) have diverse phenotypes across different tissues and disease states. Recent insights into ILC2 biology raise new possibilities for the improved treatment of cancer and of metabolic, infectious and chronic inflammatory diseases.

Innate lymphoid cell (ILC) subsets with defined phenotypes can adapt to local environmental cues through transdifferentiation. Studies of such plasticity have improved our understanding of the biological roles of ILCs and offer promise for new strategies to treat inflammatory diseases and cancer.

Kwakkenbos et al. describe an in vitro method to generate antibody-secreting B cell lines from human peripheral blood memory B cells by transducing them with retroviral vectors encoding Bcl-6 and Bcl-xL. The approach can be used to stably and simultaneously produce high levels of B cell receptor (BCR) on the cell surface and secreted immunoglobulins, useful for studying BCR signaling and producing antigen-specific antibodies.

Analyses of tumour samples and tumour-infiltrating lymphocytes from two patients with melanoma who were treated with adoptive T-cell therapy provide evidence for tumour escape by loss and downregulation of immunogenic antigens.

A recent paper published in Nature demonstrates a multifaceted relation between enteric glial cells (EGC), intestinal epithelia, and ILC3, via the EGC release of neurotrophic factors, a structurally related group of ligands within the TGF-β superfamily of signaling molecules and IL-22 produced by ILC3.

The lack of robust and high-throughput technologies to analyze the human TCR repertoire has been a bottleneck in the analysis of human T cell responses. Linnemann and colleagues have addressed this issue by using a TCR gene capture technology that, because of its quantitative nature, allows the rapid identification of TCRab pairs from bulk populations of cells without the need for single-cell cloning. Such an approach should be useful in obtaining defined antigen-reactive TCRs for therapeutic purposes.