Volume 13 Issue 8, August 2012

The sensing of viral infection by the innate immune system is dominated by the recognition of nucleic acids. New data now demonstrate that the fusion of viral and target-cell membranes leads to the activation of an immune response dependent on the adaptor STING.

Substantial depletion of Langerhans cells leads to their replenishment by bone marrow–derived precursors that access the epidermis through hair follicles, a site of crucial chemokine production.

Most myeloid cells express the growth-factor receptor CSF1R. Recognition of interleukin 34 by CSF1R is required for the development of tissue-resident Langerhans cells and microglia, which explains the independence of their growth from CSF1.

The transcription factor Aiolos is upregulated in T lymphocytes in a manner dependent on the transcription factors STAT3 and AhR and leads to epigenetic silencing of the gene encoding interleukin 2. This acts as a cell-intrinsic safeguard mechanism for the differentiation of helper T cells into the T_H17 subset.

Intestinal microfold (M) cells actively capture luminal antigens and move them by transcytosis to initiate immune responses. Ohno and colleagues show that the Ets transcription factor Spi-B is necessary for M-cell differentiation.

Fusion with the cell membrane is the earliest event in viral infection. Paludan and colleagues show that 'unscheduled' membrane-fusion events elicit an innate immune response dependent on the adaptor STING.

Hair is a skin component that functions as a physical barrier and thermal regulator. Nagao and colleagues show that hair follicles recruit Langerhans cells to the epidermis via the secretion of various chemokines.

Tissue-specific Langerhans cells and microglia develop in situ before birth. Colonna and colleagues identify IL-34 produced by keratinocytes and neurons as the relevant ligand of CSF1R necessary for their generation.

Lyl-1 is a transcription factor expressed in hematopoietic progenitors. Goodell and colleagues show that Lyl-1 is required for lymphoid specification and the maintenance of early T lineage progenitors.

IL-2 production is actively suppressed during T_H17 differentiation. Quintana and colleagues show that the transcription factor Aiolos is induced by the transcription factors STAT3 and AhR and silences the Il2 locus.

The mechanisms of TGF-β-mediated inhibition of T_H2 differentiation remain unclear. Nakayama and colleagues show that TGF-β induces the transcription factor Sox4, which negatively regulates the transcription factor GATA-3 by two independent mechanisms.

TCR microcluster signaling occurs in cognate T cells after they encounter antigen-presenting cells. Krummel and colleagues show that immune synapses are motile as microclusters coalesce after the actin depolymerization that occurs during T cell movement.