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Brief Definitive Report

Memory CD4+ T cell homeostasis and AIDS progression are independent of naive CD4+ T cells in SIV infection of nonhuman primates.

Human skin-draining lymph nodes contain functionally distinct subsets of resident and migratory dendritic cells.

Di-methylation of histone H3 at lysine 9 (H3K9me2) suppresses expression of interferon genes, and deletion or inactivation of the lysine methyltransferase G9a converts fibroblasts into interferon-producing cells resistant to RNA viruses.

MLH1 ATPase activity is essential for class switch recombination but not for somatic hypermutation.


Triple-negative breast cancers with elevated MYC are sensitized to CDK inhibition.

HSP90 inhibition depletes STK33 in KRAS mutant tumors.

Rictor is essential in Notch-driven T-ALL pathogenesis.

Notch signaling is required for the generation of α4β7+RORγt fetal progenitors, but must then be turned off to allow RORγt expression and LTi cell maturation.

In mice lacking both Mst1 and Mst2 in the lymphoid compartment, thymocyte development is normal, but single-positive thymocytes exhibit excessive apoptosis and greatly diminished thymic egress, accompanied by loss of chemokine activation of RhoA and Rac1.

Crystal structure and mutagenesis analyses suggest a MAIT TCR–MR1 docking mode distinct from the NKT TCR-CD1d docking mode.

Gain- and loss-of-function analyses reveal that the transcription factor EBF1 is required for normal differentiation and function of marginal zone, B-1, follicular, and germinal center B cells in mice.

Transglutaminase 2 is required for the development of IgA nephropathy.

The transcription factor ATF3 inhibits lipid body formation in macrophages during atherosclerosis in part by dampening the expression of cholesterol 25-hydroxylase.

Deep vein thrombosis initiation is mediated by cross talk between monocytes, neutrophils, and platelets.

The PET imaging agent CuII(atsm) improves motor and cognitive function in Parkinson’s disease.

Cells from Cockayne syndrome patients and a mouse model of the disease show increased metabolism as a result of impaired autophagy-mediated removal of damaged mitochondria.

The ER chaperone GRP78/BiP is crucial for the development of rheumatoid arthritis.

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