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Innate effector mechanisms contribute to the control of viremia and modulate the quality of the adaptive immune response to HIV-1. Altfeld and Gale discuss the concerted actions of PRR signaling, innate immune cells and innate-adaptive crosstalk that direct the outcome of HIV-1 infection.
Understanding the success and failure of the HIV-specific cellular immune response has implications for immunotherapies and vaccines for HIV-1. Migueles and Connors discuss the mechanisms that are most likely responsible for durable and potent immunologic control of HIV-1 by the cellular immune response.
The persistence of HIV reservoirs remains a barrier to sustained virologic remission in HIV-infected individuals after antiretroviral therapy is discontinued. Fauci and colleagues discuss the therapeutic strategies aimed at eliminating or controlling the virus in the absence of ART.
HIV devotes a large portion of its coding capacity to counteracting the function of mammalian antiviral proteins. Landau and colleagues discuss the biology of mammalian restriction factors and the viral accessory proteins that counteract them.
Antibody responses to the HIV-1 envelope glycoproteins can be classified into three groups. Burton and Mascola discuss how recent insight into the structure and immunology of non-neutralizing, strain-specific and broadly neutralizing antibodies guide HIV-1 vaccine design and therapeutic strategies.
The mediobasal hypothalamus detects increased amounts of tumor necrosis factor during the early phases of inflammation and relays this information to cells of the adaptive immune system by mobilizing free fatty acids.
The cell-surface receptor TREML4 amplifies cellular responses to single-stranded RNA by regulating recruitment of the adaptor MyD88 to the receptor TLR7. Mice lacking TREML4 show impaired antiviral immunity but also reduced severity of lupus-like disease.
The methyltransferase Ezh2, an epigenetic regulator associated with tumor-cell metastasis, also methlyates the cytoplasmic integrin adaptor talin. This modification inhibits the binding of talin to F-actin, which enhances the migration and invasion of dendritic cells and neutrophils.
Guanylate-binding proteins (GBPs) induced by type I interferon signaling cause lysis of Francisella bacteria that have reached the host-cell cytosol. The liberated bacterial DNA is then sensed by the cytosolic AIM2 inflammasome, which activates caspase-1 and leads to pyroptotic cell death.
IL-6 has context-dependent pro- and anti-inflammatory properties and is now regarded as a prominent target for clinical intervention. Hunter and Jones discuss the effect of IL-6 on innate and adaptive immunity, and consider how the immunobiology of IL-6 may inform clinical decisions.
Stromal cells in the subcapsular sinus of the lymph node 'decide' which cells and molecules are allowed access to the deeper parenchyma. The glycoprotein PLVAP is a crucial component of this selector function.
Interleukin 7 (IL-7) promotes the self-renewing ability of CD4− CD8− double-negative thymocytes by both supporting cell growth and repressing rearrangements of the locus encoding the T cell antigen receptor (TCR).
The transcription factor Sox2 has an additional function in neutrophils, as a cytoplasmic sensor of DNA. Upon binding bacterial DNA, Sox2 initiates a signaling cascade dependent on the kinase TAK1 and adaptor TAB2 that culminates in the expression of genes encoding pro-inflammatory molecules.
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.
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.
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.
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.
