Volume 16 Issue 6, June 2015

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.

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.

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.

An effect of host genetic variation on susceptibility to HIV-1 was identified early in the pandemic. McLaren and Carrington discuss the extent to which additional polymorphisms influence HIV-1 disease progression and how analysis of data sets may discover novel gene variants that affect the outcome of HIV-1.

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.

Due to their role in regulating DNA-methylation patterns, the TET proteins, in particular TET2, have emerged as key participants in tumorigenesis. Now the spotlight shifts to TET1 and its role as a tumor suppressor in lymphomagenesis.

Like T cells and B cells, innate lymphoid cells (ILCs) develop from common lymphoid progenitors, but how commitment to the ILC lineage is regulated has remained unclear. The transcriptional regulator TOX is important in this process.

The anti-inflammatory molecule A20 inhibits necroptotic cell death by inhibiting ubiquitination of the kinase RIPK3 at the Lys5 residue and preventing excessive formation of the RIPK1-RIPK3 necroptotic complex.

The transcriptional regulation of the differentiation of innate lymphoid cells remains incompletely characterized. Kaye and colleagues show that the transcriptional regulator TOX is required for the differentiation of common lymphoid progenitors into the innate lymphoid cell lineage.

Eosinophils are commonly observed in solid tumors, but their role has remained uncertain. Hämmerling and colleagues show that activated eosinophils contribute to tumor eradication by altering tumor vasculature and increasing the infiltration of CD8⁺ T cells.

A20 is a deubiquitinating enzyme that restrict inflammation by various mechanisms. Ma and colleagues show that A20 inhibits necroptosis by inhibiting the ubiquitination of RIPK3 and formation of the RIPK1-RIPK3 complex.

Regulatory T cells (T_reg cells) can suppress autoreactive immune responses in the periphery. Joost van Meerwijk and colleagues show that activated peripheral T_reg cells can recirculate back to the thymus, where they can suppress further thymic T_reg cell development.

Thymic regulatory T cells require IL-2 for their development. Robey and colleagues show that developing cells compete with pre-existing regulatory T cells for limiting amounts of IL-2 produced by antigen-bearing dendritic cells

Fungal infection induces signaling downstream C-type lectin receptors through the activation of the tyrosine kinase Syk. Xiao and colleagues show that the phosphatase SHP-2 recruits Syk to dectin-1.

Methylation of DNA CpG motifs is modulated in part by the TET family of epigenetic regulators. Aifantis and colleagues show that loss of TET1 function biases hematopoiesis toward the B cell lineage and promotes hematopoietic malignancies.

The process of B cell differentiation into plasma cells involves dramatic cellular reprogramming. Corcoran and colleagues profile the transcriptome of all stages of B cell differentiation through to antibody-secreting plasma cells.

Nature Immunologypresents a series of specially commissioned articles that discuss the most recent progress in understanding the immune response to HIV and how this new insight can be harnessed for prophylactic vaccines and immunotherapies.