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    ON THE COVER
    Berre et al. show that anti-CD36 treatment of HIV-infected cells induces large tethering of viral particles (purple) at the plasma membrane. Image shows an electron micrograph of HIV-infected cells (pink) treated with anti-CD36. Image enhanced by Sylvia Cuadrado (scuadrado@rockefeller.edu).
    See page 2523

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ISSN 0022-1007
EISSN 1540-9538
In this Issue

Brief Definitive Report

The cohesin complex is recruited to DNA switch regions and is required for nonhomologous end joining during immunoglobulin class switch recombination.

The cohesin loading protein is required for nonhomologous end joining of double-strand DNA breaks

Type I interferon promotes the differentiation of plasmacytoid dendritic cells in part by up-regulating expression of Flt3 on common lymphoid progenitors.

Article

Antibody targeting CD36 on HIV-1–infected macrophages results in rapid retention of virions within virus-containing compartments to inhibit release and viral transmission to T cells.

The regulation of phagocytosis previously ascribed to prion protein PrPC is found to be controlled by the linked locus encoding SIRPα.

Loss of dual leucine zipper kinase results in attenuated JNK/c-Jun stress response pathway activation and reduced neuronal degeneration after kainic acid–induced excitotoxic seizures.

A comprehensive structural portrait of the association between citrullination, the HLA-DRB1 locus, and T cell autoreactivity in rheumatoid arthritis.

IL-4–producing basophils promote the trapping of N. brasiliensis in the skin during secondary infection, a process critical for limiting the spread of infection to the lungs.

Bone morphogenetic protein 7 (BMP7) promotes the differentiation of Langerhans cells in the epidermis during prenatal development.

VEGF-driven neovascularization transiently recruits Ly6Chigh monocytes, which subsequently alter their phenotype and exert angiogenic function to enlarge small vessels.

Deletion of Ezh2 results in transcriptional repression of developmental regulator genes, derepression of oncogenic polycomb targets, and induction of MDS/MPN-like disease in mice that is exacerbated by concurrent deletion of Tet2.

Loss of Asxl1 results in myelodysplastic syndrome, whereas concomitant deletion of Tet2 restores HSC self-renewal and triggers a more severe disease phenotype distinct from that seen in single-gene knockout mice.

BCR-ABL+lineagec-kit immature leukemia cells produce inflammatory MIP-1α/CCL3 to maintain leukemia-initiating cells and promote development of chronic myeloid leukemia.

The diuretic drug spironolactone up-regulates NKG2D ligand expression in colon cancer cells via activation of the ATM–Chk2–mediated checkpoint pathway to enhance the antitumor function of NK cells.

Adenosine receptor signaling inhibits TCR-induced activation of PI3K–Akt to reduce IL-7Rα expression on T cells, thereby regulating development and maintenance of naive T cells in the periphery.

Regulation of IL-2–producing CD4+ T cell numbers is controlled by a quorum-sensing feedback loop as regulatory T cells sense the IL-2 produced.

In T cells, PI3K activation in the periphery of the immune synapse leads to PIP3 accumulation that promotes actin polymerization in a pathway important for cytotoxic function.

Memory B cells, unlike naive B cells, require a reduced level of STAT3 activation to differentiate into antibody-secreting plasmablasts in response to IL-10 and IL-21; however, this process requires IL-21R expression in both naive and memory cells.

Direct class switching to IgE generates IgE+ GC cells that are highly apoptotic and do not contribute to the memory compartment, while sequential switching through an IgG+ intermediate results in the generation of long-lived IgE+ plasma cells.

Transgenic expression of TLR7 results in the expansion and hyperactivation of T1 B cells in response to endogenous RNA complexes, leading to increased autoantibody production.

Correction

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