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Letter

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.

Wenzhong Xiao,and the Inflammation and Host Response to Injury Large-Scale Collaborative Research Program7,Michael N. Mindrinos,and the Inflammation and Host Response to Injury Large-Scale Collaborative Research Program7,Junhee Seok,and the Inflammation and Host Response to Injury Large-Scale Collaborative Research Program7,Joseph Cuschieri,and the Inflammation and Host Response to Injury Large-Scale Collaborative Research Program7,Alex G. Cuenca,and the Inflammation and Host Response to Injury Large-Scale Collaborative Research Program7,Hong Gao,and the Inflammation and Host Response to Injury Large-Scale Collaborative Research Program7,Douglas L. Hayden,and the Inflammation and Host Response to Injury Large-Scale Collaborative Research Program7,Laura Hennessy,and the Inflammation and Host Response to Injury Large-Scale Collaborative Research Program7,Ernest E. Moore,and the Inflammation and Host Response to Injury Large-Scale Collaborative Research Program7,Joseph P. Minei,and the Inflammation and Host Response to Injury Large-Scale Collaborative Research Program7,Paul E. Bankey,and the Inflammation and Host Response to Injury Large-Scale Collaborative Research Program7,Jeffrey L. Johnson,and the Inflammation and Host Response to Injury Large-Scale Collaborative Research Program7,Jason Sperry,and the Inflammation and Host Response to Injury Large-Scale Collaborative Research Program7,Avery B. Nathens,and the Inflammation and Host Response to Injury Large-Scale Collaborative Research Program7,Timothy R. Billiar,and the Inflammation and Host Response to Injury Large-Scale Collaborative Research Program7,Michael A. West,and the Inflammation and Host Response to Injury Large-Scale Collaborative Research Program7,Bernard H. Brownstein,and the Inflammation and Host Response to Injury Large-Scale Collaborative Research Program7,Philip H. Mason,and the Inflammation and Host Response to Injury Large-Scale Collaborative Research Program7,Henry V. Baker,and the Inflammation and Host Response to Injury Large-Scale Collaborative Research Program7,Celeste C. Finnerty,and the Inflammation and Host Response to Injury Large-Scale Collaborative Research Program7,Marc G. Jeschke,and the Inflammation and Host Response to Injury Large-Scale Collaborative Research Program7,M. Cecilia López,and the Inflammation and Host Response to Injury Large-Scale Collaborative Research Program7,Matthew B. Klein,and the Inflammation and Host Response to Injury Large-Scale Collaborative Research Program7,Richard L. Gamelli,and the Inflammation and Host Response to Injury Large-Scale Collaborative Research Program7,Nicole S. Gibran,and the Inflammation and Host Response to Injury Large-Scale Collaborative Research Program7,Brett Arnoldo,and the Inflammation and Host Response to Injury Large-Scale Collaborative Research Program7,Weihong Xu,and the Inflammation and Host Response to Injury Large-Scale Collaborative Research Program7,Yuping Zhang,and the Inflammation and Host Response to Injury Large-Scale Collaborative Research Program7,Steven E. Calvano,and the Inflammation and Host Response to Injury Large-Scale Collaborative Research Program7,Grace P. McDonald-Smith,and the Inflammation and Host Response to Injury Large-Scale Collaborative Research Program7,David A. Schoenfeld,and the Inflammation and Host Response to Injury Large-Scale Collaborative Research Program7,John D. Storey,and the Inflammation and Host Response to Injury Large-Scale Collaborative Research Program7,J. Perren Cobb,and the Inflammation and Host Response to Injury Large-Scale Collaborative Research Program7,H. Shaw Warren,and the Inflammation and Host Response to Injury Large-Scale Collaborative Research Program7,Lyle L. Moldawer,and the Inflammation and Host Response to Injury Large-Scale Collaborative Research Program7,David N. Herndon,and the Inflammation and Host Response to Injury Large-Scale Collaborative Research Program7,Stephen F. Lowry,and the Inflammation and Host Response to Injury Large-Scale Collaborative Research Program7,Ronald V. Maier,and the Inflammation and Host Response to Injury Large-Scale Collaborative Research Program7,Ronald W. Davis,and the Inflammation and Host Response to Injury Large-Scale Collaborative Research Program7,Ronald G. Tompkins,and the Inflammation and Host Response to Injury Large-Scale Collaborative Research Program7

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 have the unique capacity to recognize variants of West Nile virus, likely providing protection against mutant viruses that escape antibody neutralization.

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.

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.

Article

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.

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.

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.

Correction

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