ON THE COVER
Séror et al. find that encounter with the HIV-1 envelope glycoprotein complex (Env) prompts target cells to release ATP through pannexin-1 channels. Extracellular ATP then triggers purinergic receptor signaling, which facilitates target cell infection by HIV-1. Image depicts an abstraction of HeLa cells engineered to express CXCR4 and CD4 (green) or HIV-1 Env (purple). Artwork by Lewis Long.
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Brief Definitive Report
CD1b tetramers bind αβ T cell receptors to identify a mycobacterial glycolipid-reactive T cell repertoire in humans
Glucose monomycolate–loaded CD1b tetramers identify a subset of CD4+ T cells in patients with Mycobacterium tuberculosis infection.
Deletion of Roquin in T or B cells, or in the entire hematopoietic system of mice, alters immune homeostasis but does not result in autoimmunity.
The Paf oncogene is highly expressed in cycling hematopoietic stem cells (HSCs) and is required for the development of long-term HSCs.
Immune cell activation induces concurrent temporal and spatial retinoic acid signaling, and CD4+ T cell–specific loss of RA signals reduces effector function, migration, and polarity.
Differential regulation of mast cell degranulation versus cytokine secretion by the actin regulatory proteins Coronin1a and Coronin1b
Coronin1a inhibits mast cell degranulation through actin cytoskeletal dynamics while augmenting cytokine secretion, an effect exacerbated by additional loss of Coronin1b.
CD103+ pulmonary dendritic cells preferentially acquire and present apoptotic cell–associated antigen
CD103-expressing dendritic cells in the lungs preferentially take up and cross-present antigen from apoptotic cells.
Targeting cap-dependent translation blocks converging survival signals by AKT and PIM kinases in lymphoma
PIM kinase expression in human lymphomas can influence the outcome of chemotherapy, and blocking cap-dependent translation can reverse PIM-mediated rapamycin resistance in murine lymphomas.
High-level IGF1R expression is required for leukemia-initiating cell activity in T-ALL and is supported by Notch signaling
Notch-driven expression of IGF1R promotes the growth, viability, and transplantability of T-ALL cells.
Contact with HIV-1 envelope protein elicits release of ATP through pannexin-1 channels on target cells; by activating purinergic receptors and Pyk2 kinase in target cells, this extracellular ATP boosts HIV-1 infectivity.
As revealed in a new model of cerebral cavernous malformations (CCM), the timing of ablation of Ccm genes determines whether or not CCM lesions arise in brain and retina venous beds.
Anti–IL-20 monoclonal antibody inhibits the differentiation of osteoclasts and protects against osteoporotic bone loss
IL-20 promotes osteoclast differentiation by inducing RANK and RANKL expression in osteoclast precursors and osteoblasts, respectively.
Preexisting helminth infection induces inhibition of innate pulmonary anti-tuberculosis defense by engaging the IL-4 receptor pathway
Preexisting helminth infection impairs immunity against subsequent M. tuberculosis infection, in part by inducing alternatively activated macrophages.
Cytokine signals through PI-3 kinase pathway modulate Th17 cytokine production by CCR6+ human memory T cells
PI-3K–mediated repression of FOXO1 and KLF2 promotes proinflammatory cytokine expression by lineage-committed human CCR6+ Th17/Th22 memory cells.
Constitutive intestinal NF-κB does not trigger destructive inflammation unless accompanied by MAPK activation
Constitutive NF-κB activation in IECs induces inflammatory cytokines and chemokines in the lamina propria, but does not result in overt tissue damage unless acute inflammatory insults are present, causing TNF-dependent destruction and barrier disruption.
CSF-1 drives the homeostatic expansion of macrophages within the growing myometrium of pregnant mice by stimulating in situ proliferation and inducing monocyte precursor recruitment from the blood.
NIK signaling in dendritic cells but not in T cells is required for the development of effector T cells and cell-mediated immune responses
NIK expression in thymic dendritic cells is required for the development of effector T cells and their ability to promote EAE.