The business of midwifery: documentation for success III--homebirth.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to Linda Lieberman.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
RelB, a member of the NF-kappaB family of transcription factors, is essential for dendritic cell (DC) maturation. Recent findings indicate that RelB is exclusively regulated through its interaction with cytoplasmic NF-kappaB2/p100. The studies presented in this report show that DCs lacking NF-kappaB2 have dramatically enhanced RelB activity, associated with increased MHC class II and costimulatory molecule expression and an enhanced ability to induce CD4(+) T cell responses. These studies identify a novel role for NF-kappaB2 in the negative regulation of RelB-induced DC maturation, with critical consequences for the regulation of adaptive immune responses.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Although recent studies have described IL-27 and its receptor, WSX-1, as promoters of Th1 differentiation in naive CD4+ T cells, the data presented here indicate that signaling through this receptor is involved in limiting the intensity and duration of T cell activity. When WSX-1-deficient mice are infected with the intracellular pathogen Toxoplasma gondii, they establish protective T cell responses, characterized by production of inflammatory cytokines and control of parasite replication. However, infected WSX-1-/- mice are unable to downregulate these protective responses, and develop a lethal, T cell-mediated inflammatory disease. This pathology was characterized by the excessive production of IFN-gamma, persistence of highly activated T cells, and enhanced T cell proliferation in vivo. Together, these findings demonstrate that WSX-1 is not required for the generation of IFN-gamma-mediated immunity to this parasitic infection and identify a novel function for this receptor as a potent antagonist of T cell-mediated, immune hyperactivity.