Brief Definitive Report
Loss of antiproliferative gene TOB1 results in more severe EAE driven by augmented pathogenic T cell responses.
Therapeutic targeting of NOTCH signaling ameliorates immune-mediated bone marrow failure of aplastic anemia
Notch1 signaling sustains the proinflammatory behavior of Th1 cells, implicated in the development of aplastic anemia in humans and mice.
The transcription factor AP4 is a critical regulator of epithelial–mesenchymal transition, migration, invasion, and metastasis in colorectal cancer cells.
PDGFRα and CD51 mark human Nestin+ sphere-forming mesenchymal stem cells capable of hematopoietic progenitor cell expansion
A subset of human Nestin+ mesenchymal stem cells expresses PDGFRα and CD51, and these markers can be used for prospective isolation of these cells.
The Human papillomavirus type 16 E7 oncoprotein induces a transcriptional repressor complex on the Toll-like receptor 9 promoter
HPV16-positive cervical cancer lesions contain NFκB–ERα nuclear complexes to repress the TLR9 promoter.
Indoleamine 2,3-dioxygenase is a critical resistance mechanism in antitumor T cell immunotherapy targeting CTLA-4
Indoleamine 2,3-dioxygenase suppresses infiltration and accumulation of tumor-reactive T cells in the context of anti–CTLA-4 immunotherapy and attenuates the anti-tumor efficacy.
Identification of beryllium-dependent peptides recognized by CD4+ T cells in chronic beryllium disease
Identification of peptides that form complexes with beryllium and class II HLA molecules and are recognized by CD4+ T cells from patients with chronic beryllium disease.
MDSC-derived nitric oxide supports the development of Th17 cells in ovarian cancer dependent on the induction of endogenous NOS2 and the cGMP–cGK pathway in Th17 cells.
Nitric oxide derived from iNOS in activated T cells negatively regulates Th17 cell differentiation.
N-ras couples antigen receptor signaling to Eomesodermin and to functional CD8+ T cell memory but not to effector differentiation
N-ras−/− CD8+ T cells have an intrinsic defect in Eomes expression resulting in impaired generation of protective memory cells that can be rescued by enforced Eomes expression.
Ongoing transcription of the Ig gene coupled with temporary pausing within the targeted region facilitates somatic hypermutation.