These results suggest that either the production of specific antibodies amplified quickly to sufficient levels after the second encounter with VACV or that the control of virus spread was Nomifensine Maleate mediated mostly by cellular immunity. Nevertheless both wildtype, replicating strains of VACV and MVA were previously shown to induce apoptosis of dendritic cells and thus affect their antigen-presenting function as well as other PJ34 immune responses. In any case, regardless of the exact mechanisms involved, our results prove the usefulness and efficiency of the immunization with MVA in an atopic organism. Probably, this efficiency could be further improved if a protocol consisting of several consecutive doses of MVA was used. For obvious reasons, the mounting of protective responses against smallpox cannot be tested in human, but the re-introduction of vaccination of the general population still has been considered. Our work thus supports usefulness and efficacy of MVA-based vaccines against lethal poxviral infection also in an atopic organism. To gain further insight into IQGAP2 expression in human IBD and colorectal cancer, we conducted an extensive meta-analysis of published RNA microarray datasets. The results of this analysis are summarized inS1 Table. Among eight different studies, which had data on Iqgap2 available, comparing RNA transcript expression profiles of IBD colonic biopsies and either healthy controls or adjacent unaffected colonic tissue, Iqgap2 levels were minimally decreased in IBD versus either healthy or ��unaffected�� colonic tissue. IBD is a multifactorial disease and the molecular mechanisms driving its pathogenesis are still not fully understood. Previous studies identified IQGAP2 as a tumor suppressor in liver and stomach and as a mediator of several major signaling pathways ], although until no wits role in gastrointestinal inflammation has not been addressed. Here we report that IQGAP2 is required for the development of acute colitis in mice. We found that Iqgap2-/- mice were protected from colonic injury in the DSS-induced colitis model. Protection from colitis in Iqgap2-/- mice was evident by maintenance of normal body weight, absence of hematochezia and intact colonic epithelium and crypt architecture. While IQGAP2 appears dispensable for normal colonic homeostasis, upon exposure to DSS, Iqgap2-/- colonic mucosa displayed suppressed NF-��B activation and low levels of TLR4, MyD88, IL-6 and pSTAT3 compared to mucosa from DSS-treated WT mice.