Anna Ridderstad

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Background and aims: Dextran sulfate sodium (DSS) induced colitis exhibits a predominantly NF-κB dependent proinflammatory cytokine profile and shares similarities with human inflammatory bowel disease (IBD). Lamina propria macrophages of IBD patients display elevated levels of NF-κB p65. Knowing the role of NF-κB in IBD, we investigated the beneficial(More)
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(More)
In this study, we examine the relationship between primary and secondary T cell-dependent immune responses using the response of xid mice to the hapten (4-hydroxy-3-nitrophenyl)acetyl (NP) as an experimental model. The reduced serologic primary immune response of xid mice was demonstrated to be caused by a substantially decreased Ab-forming cell (AFC)(More)
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(More)
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(More)
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(More)
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