A constitutively active aryl hydrocarbon receptor causes loss of peritoneal B1 cells.

The dioxin/aryl hydrocarbon (Ah) receptor functions as a ligand-activated transcription factor that mediates toxicity of dioxins and related environmental pollutants. We have developed a transgenic mouse model that expresses a constitutively active Ah receptor. The immune system is one of the most sensitive target organs for dioxin toxicity and we have therefore investigated alterations of different lymphocyte populations in these mice.

Abrogated lymphocyte infiltration and lowered CD14 in dextran sulfate induced colitis in mice treated with p65 antisense oligonucleotides.

Background And Aims: Dextran sulfate sodium (DSS) induced colitis exhibits a predominantly NF-kappaB dependent proinflammatory cytokine profile and shares similarities with human inflammatory bowel disease (IBD). Lamina propria macrophages of IBD patients display elevated levels of NF-kappaB p65. Knowing the role of NF-kappaB in IBD, we investigated the beneficial cellular mechanisms underlying the lasting effect of a single p65 antisense treatment in DSS-colitis mice.

Interference of eukaryotic signalling pathways by the bacteria Yersinia outer protein YopJ.

Upon contact with bacteria, eukaryotic cells activates a slurry of defence mechanisms via distinct signalling transduction pathways. However, some bacteria have evolved strategies to escape or inhibit these host defence systems. We have recently shown that the bacteria Yersinia pseudotuberculosis, which encodes the Yersinia outer protein (YopJ) appears to inhibit the activation of NF-kappaB by preventing the phosphorylation of IkappaB.

Kinetics of establishing the memory B cell population as revealed by CD38 expression.

In this report, we detail changes in the expression of CD38 on murine B cells during the course of a T cell-dependent immune response. CD38 is expressed on all naive B cells but is down-regulated on isotype-switched B cells from both the germinal centers (GCs) and the foci of Ab-forming cells which arise during the first weeks of the response. The down-regulation on GC B cells, however, is reversible since Ag-specific IgG1 B cells with high levels of CD38 are apparent by 2 wk postimmunization.

B cell memory in xid mice is long-lived despite reduced memory B cell frequency.

Brutons tyrosine kinase (Btk) deficient xid mice have a diminished primary T cell dependent immune response, resulting in a reduced memory B cell frequency. Boosting at 35 days post primary immunization, however, generates a normal secondary immune response, indicating a functional memory B cell compartment. The longevity of B cell memory appears to depend on both the presence of antigen and expression of cell survival genes such as bcl-2.