Susan Shinton

Human chronic lymphocytic leukemia modeled in mouse by targeted TCL1 expression.

Positive selection of anti-thy-1 autoreactive B-1 cells and natural serum autoantibody production independent from bone marrow B cell development.

Characterization of B lymphopoiesis in mouse bone marrow and spleen.

Association of B-1 B cells with follicular dendritic cells in spleen.

Evidence of marginal-zone B cell-positive selection in spleen.

Lineage specification and plasticity in CD19- early B cell precursors.

Autoreactive B-1 B cells: constraints on natural autoantibody B cell antigen receptors.

Biallelic, ubiquitous transcription from the distal germline Ig{kappa} locus promoter during B cell development.

Mice heterozygous for germ-line mutations in methylthioadenosine phosphorylase (MTAP) die prematurely of T-cell lymphoma.

Natural anti-intestinal goblet cell autoantibody production from marginal zone B cells.

Lin28b promotes fetal B lymphopoiesis through the transcription factor Arid3a.

B cells generated by B-1 development can progress to chronic lymphocytic leukemia.

A developmental switch between fetal and adult B lymphopoiesis.

Mutagenesis Screen Identifies agtpbp1 and eps15L1 as Essential for T lymphocyte Development in Zebrafish.

Loss of a chromosomal region with synteny to human 13q14 occurs in mouse chronic lymphocytic leukemia that originates from early-generated B-1 B cells.

Early generated B1 B cells with restricted BCRs become chronic lymphocytic leukemia with continued c-Myc and low Bmf expression.

Zebrafish B Cell Development without a Pre-B Cell Stage, Revealed by CD79 Fluorescence Reporter Transgenes.

NLR Nod1 signaling promotes survival of BCR-engaged mature B cells through up-regulated Nod1 as a positive outcome.

Early Generated B-1-Derived B Cells Have the Capacity To Progress To Become Mantle Cell Lymphoma-like Neoplasia in Aged Mice.

The cis-Regulatory Atlas of the Mouse Immune System.

Crucial Role of Increased Arid3a at the Pre-B and Immature B Cell Stages for B1a Cell Generation.

Investigation of the causal etiology in a patient with T-B+NK+ immunodeficiency.

Pla2g2a promotes innate Th2-type immunity lymphocytes to increase B1a cells.

B-1 derived anti-Thy-1 B cells in old aged mice develop lymphoma/leukemia with high expression of CD11b and Hamp2 that different from TCL1 transgenic mice.

E proteins control the development of NKγδT cells through their invariant T cell receptor.