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Brief Definitive Report

Fanca contributes to both somatic hypermutation and class switch recombination events in splenic B cells.

Immune responses can be predicted by the chemical properties of systematically variable inorganic crystalline materials.

In contrast to BRCA1, CtIP has indispensable roles in promoting resection and embryonic development.


Axonal guidance molecule netrin-1 promotes resolution of inflammation, with netrin-1 and resolvin D1 mutually inducing each other’s expression.

Pharmacological disruption of the interaction between fibrinogen and β-amyloid reduces vascular amyloid deposition and improves cognition in a mouse model of Alzheimer’s disease.

Endogenous 12-HHT, or a synthetic BLT2 agonist promotes epidermal wound closure by stimulating BLT2 on keratinocytes, inducing TNF and MMP production.

A conserved regulatory element in intron 1 of UNC13D regulates Munc13-4 expression.

TNF signaling inactivation sensitizes AML cells to NF-kB inhibition but protects healthy hematopoietic stem progenitor cells from this treatment.

The lymph node follicular dendritic cell (FDC) network is derived from the expansion and differentiation of marginal reticular cells, as are the new FDCs generated during an immune response.

In vivo FRET demonstrates that ERK positively regulates the neutrophil recruitment cascade in the intestine by promoting adhesion and migration.

Bcl6 and E3 ligase cullin 3 complexes mediate negative feedback regulation during thymocyte development and T cell activation to restrain exaggerated Tfh responses.

LNSCs present peptide–MHCII complexes acquired from DCs to CD4+ T cells and induce T cell dysfunction by preventing their proliferation and survival.

Neuropilin 1 regulates angiogenesis in a VEGF-independent manner via association with ABL1, suggesting that Imatinib represents a novel opportunity for anti-angiogenic therapy.

Fractalkine interactions with its receptor, CX3CR1, regulate CD4+ T cell retention in atopic dermatitis and offer a potential therapeutic target in allergic disease.

Bacteria can utilize a mammalian host siderophore to usurp host iron; however, the host can respond by down-regulating siderophore expression and up-regulating expression of an inhibitory siderophore-binding protein.

Shigella flexneri interacts with B cells and induces apoptosis via IpaD binding to TLR2.

Siglec-5 and Siglec-14 are shown to be paired inhibitory/activating receptors expressed on neutrophils and amniotic epithelium and modulating immune responses to group B Streptococcus.

In response to lung infection, pleural innate response activator B cells produce GM-CSF–dependent IgM and ensure a frontline defense against bacterial invasion.

Distinct mechanisms of p38 activation have opposing effects on T cell responses through differential regulation of NFATc1 activity.

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