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    Hara-Chikuma et al. demonstrate that the water/glycerol channel aquaporin-3 (AQP3) regulates chemokine-dependent trafficking of T cells to inflamed skin via uptake of hydrogen peroxide (H2O2). Image shows an abstraction of T cells (green) expressing AQP3 receptors (blue) with H2O2 uptake (yellow) migrating to the skin (red). Artwork by Rachel Urkowitz (
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ISSN 0022-1007
EISSN 1540-9538
In this Issue

Brief Definitive Report

TRAF-interacting protein (TRIP) negatively regulates TLR3/4- and RIG-I–induced IFN-β signaling by promoting K48-linked ubiquitination and proteasomal degradation of TBK1.

Neuropilin-1 is identified as a surface marker to distinguish different Foxp3+ T reg cell subsets under homeostatic conditions.


Neuropilin-1 surface expression discriminates between nT reg cells with stable expression and Nrp1 low iT reg cells showing inducible expression under inflammatory conditions.

The water/glycerol channel aquaporin-3 is required for chemokine-dependent T cell migration during immune responses.

Schistosome ribonuclease Omega-1 primes DCs to generate Th2 responses by binding and internalization by the mannose receptor and by subsequently impairing protein synthesis.

Autoimmunity occurs because central and peripheral tolerance mechanisms fail to tolerize T cells with weak self-reactivity to tissue-restricted antigen.

TCR signal attenuation selectively favors Foxp3 expression and T reg cell lineage commitment.

Dual–light chain–expressing B cells in autoimmune prone mice increase with age, contribute to the memory and plasma cell compartments, and are autoreactive.

Macrophage production of CXCL10 amplifies the production of IL-6 by B cells, leading to plasma cell differentiation.

DCIR2+ DCs can initiate extrafollicular B cell responses to T cell–dependent antigen.

A novel Bcl6 reporter mouse is used to dissect the developmental requirements, plasticity, and genetic profile of Tfh cells.

Late activator antigen-presenting cells promote Tfh differentiation of antigen-primed CD4+ T cells and antibody responses in influenza A virus infection.

In the absence of adaptive immunity, NK cells polarize M1 macrophages to facilitate cancer immunoediting.

Inhibition of macrophage SIRPα–CD47 interactions mediates phagocytosis and clearance of acute myeloid leukemia stem cells.


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