ON THE COVER
Ouchi et al. demonstrate that epidermal Langerhans cells are able to take up antigen through intact tight junctions and drive neutralizing antibody production specific for Staphylococcus aureus–derived exfoliative toxin (ET). Dermal dendritic cells are not required for this response. The authors’ original image shows a hematoxylin and eosin staining of the ear skin of mice subjected to patch immunization with recombinant ET.
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Brief Definitive Report
A substantial proportion of adult T-ALL samples display gene expression and mutation characteristics of both T cell and acute myeloid leukemias; mutations in ETV6 are found exclusively within this new molecular subgroup of adult T-ALL patients.
Critical injury in humans induces a genomic storm with simultaneous changes in expression of innate and adaptive immunity genes.
Human B1 cells can be divided, based on surface CD11b expression, into two transcriptionally and functionally distinct subsets, one of which is more abundant in lupus patients than healthy individuals.
Memory B cells, but not long-lived plasma cells, possess antigen specificities for viral escape mutants
Memory B cells have the unique capacity to recognize variants of West Nile virus, likely providing protection against mutant viruses that escape antibody neutralization.
Langerhans cell antigen capture through tight junctions confers preemptive immunity in experimental staphylococcal scalded skin syndrome
Epidermal LCs but not dermal DCs take up skin surface protein through intact tight junctions and mediate IgG1 antibody responses to bacterial antigen, conferring protective immunization.
Expression of the MAP kinase kinase kinase TAK1 in brain endothelial cells is needed for production of prostaglandin E2, and for induction of fever and sickness behavior, in response to peripheral inflammation.
Autophagy in antigen-presenting cells results in presentation of citrullinated peptides to CD4 T cells
Citrullinated peptide presentation by DCs and macrophages is constitutive, whereas B cells present modified peptides only with autophagy induced by serum starvation or BCR ligation.
By retaining NKG2D ligands within tumor cells, carcinoembryonic antigen–related cell adhesion molecule 1 (CEACAM1) facilitates tumor cell escape from NK cell–mediated cytolysis in vitro and in vivo.
BMP7 released by bone marrow stromal cells induces reversible senescence of prostate cancer stem-like cells, and BMPR2 expression inversely correlates with bone metastasis and recurrence in prostate cancer patients.
In glioblastoma multiforme, an EGFR–GBP1–matrix metalloproteinase-1 cascade drives tumor invasion but does not alter tumor proliferation, survival, or angiogenesis.
A genome-wide RNAi screen in mouse embryonic stem cells identifies Mp1 as a key mediator of differentiation
Knockdown of the scaffolding protein Mek binding protein 1 (Mp1) in mouse embryonic stem cells suppresses differentiation but not proliferation, and more invasive human germ cell tumors express lower amounts of Mp1.
As shown using clonal assays, the mouse HSC population undergoes quantitative as well as qualitative changes with age, including lineage differentiation, HSC pool size, marrow-homing efficiency, and self-renewal.
Host innate recognition of an intestinal bacterial pathogen induces TRIF-dependent protective immunity
TRIF signaling triggers the amplification of macrophage bactericidal activity sufficient to eliminate invading intestinal pathogens through the sequential induction of IFN-β and IFN-γ from macrophages and NK cells, respectively.
miR-150 promotes NK cell development and interferes with iNKT cell development due to the targeting the transcription factor c-Myb.
To be added.
As revealed by population genetic analyses, different human interferon genes evolved under distinct selective constraints and signatures of positive selection vary according to geographic region, suggesting that some sequence changes may have conferred an advantage by increasing resistance to viral infection.