- Lyst links endosomal trafficking to TLR function
Westphal et al. demonstrate a role of lysosomal trafficking regulator Lyst that couples the regulation of endolysosomal trafficking to inflammatory responses by the control of toll-like receptor–mediated endosomal TRIF signaling pathways.
- Niche WNT5a regulates HSC regeneration
Schreck et al. show that environmental Wnt5a regulates the transcriptome of HSCs during regeneration, particularly the expression of actin-regulatory mediators. In this manner, the niche affects engraftment through regulation of adhesion, migration, and homing of both normal and malignant cells.
- DCs in Th2 responses
Connor et al. show that transcriptomic profiling of DCs exposed to two different Th2 stimuli in vivo reveals large numbers of differentially expressed genes but few similarities between conditions.
- L. reuteri rescues scurfy mice via inosine-A2A receptors
He et al. show that T reg deficiency markedly induces autoimmunity and shifts gut microbiota. Remodeling microbiota by Lactobacillus reuteri was found to inhibit autoimmunity via the metabolite inosine, which interacts with the adenosine A2A receptor. This finding establishes a link between the gut microbiota, A2A receptors, and autoimmunity induced by T reg cell deficiency.
- Human CD70 deficiency
Abolhassani et al. show that CD70 deficiency is a novel cause of combined immunodeficiency and EBV-associated diseases, reminiscent of CD27 deficiency. CD70–CD27 interactions play a nonredundant role regulating humoral- and cell-mediated immunity in humans, especially for control of EBV.
- AhR brakes B cell effector responses
Vaidyanathan et al. report that the environmental sensor aryl hydrocarbon receptor is inducibly expressed in B cells downstream of BCR signaling and that it controls B cell fates by negatively modulating class switching and plasma cell differentiation via aicda and prdm1, respectively.
- CD70–CD27 pathway in immunity to EBV
Izawa et al. identify the first patient with CD70 deficiency suffering from recurrent EBV-induced B cell proliferations including Hodgkin’s lymphoma. Expression of CD70 on B cells is necessary to induce proliferation of EBV-specific T cells.