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Intracellular bacteria have evolved sophisticated strategies to subvert the innate immune system, which allows them to survive inside macrophages for long periods. Liu and colleagues (p 237) demonstrate that Mycobacterium tuberculosis secretes the protein phosphatase PtpA, which is activated by host ubiquitin, to suppress innate immunity. Original image by Jing Wang and Cui Hua Liu shows a HeLa cell co-transfected with vectors encoding green fluorescent protein (green) and hemagglutinin-tagged ubiquitin (red).Artwork by Cameron Long and Lewis Long.
There are clear epidemiological links between nutrition and immunological function, but a dearth of mechanistic insights has made this topic controversial. Veldhoen and Veiga-Fernandes discuss this controversy and explore ways to take this research forward.
Sequencing studies have provided a comprehensive catalog of the expression of intergenic long noncoding RNAs (lincRNAs) in 13 subsets of human T cells and B cells. Subtype-selective lincRNAs are among those identified, including linc-MAF-4, that might regulate T cell differentiation.
Genome-wide transcriptional profiling of tissue-resident innate lymphoid cells (ILCs) has provided important insight not only into their developmental relationships and phenotypic plasticity but also into previously unknown functions.
Optimal immunosuppression by regulatory T cells (Treg cells) relies on gene-expression and signaling modules that are customized to the target cell. The kinase CK2 is upregulated in Treg cells and controls a newly identified Treg cell subset that acts on dendritic cells to suppress T helper type 2 inflammatory responses in the lungs.
Direct antagonism between interleukin1 (IL-1) and the vitamin A metabolite retinoic acid tips the balance between differentiation into the TH17 subset of helper T cells or into regulatory T cells by influencing the transcription factors STAT3 and STAT5.
Alzheimer's disease is the most common dementing illness. Heneka, Golenbock and Latz review the inflammatory basis of this disease and the important role played by cells of the innate immune system.
PtpA is a secreted mycobacterial protein and virulence factor. Liu and colleagues demonstrate that PtpA suppresses signaling by cells of the innate immune system by coopting the activity of host ubiquitin.
Inflammation needs to be carefully controlled to prevent immunopathology. Zhou and colleagues demonstrate that the kinase MST4 dampens inflammation in a nonredundant way by targeting the activity of the key proinflammatory signaling molecule TRAF6.
CD1a presents a broad repertoire of lipid-based antigens. Rossjohn and colleagues show that the TCR docks over CD1a in a manner that precludes contact with permissive antigens, while nonpermissive antigens disrupt the TCR-CD1a contact.
The mechanisms that control the suppressive function of Treg cells in specific tissues are unclear. Bopp and colleagues show that Treg cells have high expression of kinase CK2 and this is critical for their ability to suppress type 2 responses in the lungs.
Obesity-associated inflammation is restrained by regulatory T cells present in visceral fat. Kallies and colleagues show interleukin 33 and the transcription factors BATF and IRF4 are necessary to maintain visceral adipose tissue Treg cells.
iTreg cells and TH17 cells share developmental steps, but their cellular fate depends on environmental cues. Weaver and colleagues show that IL-1 signaling alters the STAT3-STAT5 balance to skew cellular differentiation towards TH17 CD4+ T cells.
The mechanisms of secondary changes in antibody repertoires remain unclear. McHeyzer-Williams and colleagues define the stages of reentry of class-switched memory B cells into germinal centers to remodel existing antibody specificities.
The classification of some subsets of innate lymphoid cells (ILCs) is unclear. Colonna and colleagues use transcriptional profiling to show unique gene-expression patterns for some ILCs and overlapping patterns between ILC1 and NK cells.
Long intergenic noncoding RNAs (lincRNAs) contribute to the regulation of gene expression. Pagani and colleagues identify hundreds of unique lincRNAs expressed in human lymphocytes and demonstrate a role for the lincRNA linc-MAF-4 in the differentiation of CD4+ T cells.