Haiyan S. Li

Detection of thyroglobulin mRNA as truncated isoform(s) in mouse thymus.

Tolerogenic semimature dendritic cells suppress experimental autoimmune thyroiditis by activation of thyroglobulin-specific CD4+CD25+ T cells.

Iodination of tyrosyls in thyroglobulin generates neoantigenic determinants that cause thyroiditis.

Modifying effects of iodine on the immunogenicity of thyroglobulin peptides.

Induction of goitrous hypothyroidism by dietary iodide in SJL mice.

Variable influences of iodine on the T-cell recognition of a single thyroglobulin epitope.

Genetic complexity of autoimmune myocarditis.

Genetic differences in bone marrow-derived lymphoid lineages control susceptibility to experimental autoimmune myocarditis.

A locus on chromosome 1 promotes susceptibility of experimental autoimmune myocarditis and lymphocyte cell death.

STAT3 controls the neutrophil migratory response to CXCR2 ligands by direct activation of G-CSF-induced CXCR2 expression and via modulation of CXCR2 signal transduction.

STAT3 controls myeloid progenitor growth during emergency granulopoiesis.

Cell-intrinsic role for IFN-α-STAT1 signals in regulating murine Peyer patch plasmacytoid dendritic cells and conditioning an inflammatory response.

The transcriptional regulators Id2 and Id3 control the formation of distinct memory CD8+ T cell subsets.

STAT5 protein negatively regulates T follicular helper (Tfh) cell generation and function.

A STATus report on DC development.

G-CSF-activated STAT3 enhances production of the chemokine MIP-2 in bone marrow neutrophils.

The signal transducers STAT5 and STAT3 control expression of Id2 and E2-2 during dendritic cell development.

BRAF inhibition increases tumor infiltration by T cells and enhances the antitumor activity of adoptive immunotherapy in mice.

miR-22 controls Irf8 mRNA abundance and murine dendritic cell development.

Diversification of dendritic cell subsets: Emerging roles for STAT proteins.