This colony of transgenic mice that over-express the rat HER-2/neu oncogene under the MMTV promoter were used to study new strategies of DC-based and other therapies for advanced breast cancer. Founders were provided by Forni, Torino IT.

These mice were used in a DC staining experiment. We have started to visualize and characterize the DC which carry I-Ad/LACK complexes at the cell surface in BALB/c mice infected by leishmania major.

These not immunized mice were used in a DC staining experiment. To investigate whether several mAb could be used to detect APC presenting LACK in vivo, BALB/c mice were immunized or not with either LACK or OVA. LN cells were purified 2 days later, and stained with either 2C44, 2F74, 2E60 or 2X8 mAb. None of these mAb stained DC purified from non immunized mice. However, among the 4 mAb, only 2C44 could stain DC in LACK-immunized mice, but not in OVA-immunized mice. Furthermore, 2C44 stained DC from LACK-immunized mice expressing the H2-d haplotype but did no...

These mice were immunized with OVA and used in a DC staining experiment. LN cells were purified 2 days later, and stained with either 2C44, 2F74, 2E60 or 2X8 mAb. None of these mAb stained DC purified from non immunized mice. However, among the 4 mAb, only 2C44 could stain DC in LACK-immunized mice, but not in OVA-immunized mice.

We have attempted to identify the antigen-presenting cells (APCs) that are responsible for the development of immune tolerance in mice that have been breast-fed by antigen-exposed lactating mothers. Recent experiments performed in our laboratory have shown that the exposure of a mother to an airborne antigen during lactation impacts asthma development in their progeny. We found that airborne allergens were efficiently transferred from the mother to the neonate through the milk and that this transfer resulted in the development of antigen-specific tolerance.

These mice were studied with regard to responses to viral infections and compared to TLR K/O mice. We used the mouse pox virus Ectromelia and MVA-BN.

We found that the cooperation between IFNalpha,beta and Flt3L (FL) plays an important role in the defense against Herpes simplex virus type 1 (HSV-1) in neonates. Treatment of neonatal mice with recombinant IFNalpha has a short-term, FL-independent and a long-term, FL-dependent protective effect against HSV-1. In mice lacking FL, neonatal resistance against HSV-1 is very low and DC numbers in the spleen are reduced. In C57BL/6 mice, treatment with rIFNalpha at birth induced both FL and plasmacytoid DC (pDC) that resulted in enhanced resistance against HSV-...

We found that CCR6–deficient (CCR6-KO) mice were resistant to induction of EAE but became susceptible when transferred with small number of CCR6-sufficient T cells. CCR6 was found to be required on a first wave of TH-17 cells that entered the CNS through the choroid plexus epithelial cells, which constitutively expressed CCL20 in both mice and humans.

Experiments using these mice and IL-7R blocking antibody were carried out on the phases of cytotoxic T lymphocyte (CTL) responses.

CX3CR1 GFP mice, in which bmDC are green fluorescent (GFP), were analyzed according to their bmDC localization. It was found that the cells were organized in unique clusters, mainly located in the endosteum of the BM. These DC co-localize with B cells and these clusters are occupying architecturally definable niches and are reminiscent to the niches that were found in the cranial BM parenchyma.

These animals were used to test the combined effects of these cytokines on DC development in vivo.

These mice were generated with the intention to elucidate in vivo DC developmental regions in steady state and inflammation in situ.

We found a novel M-CSF dependent DC developmental pathway that is independent of Flt3L. These DC have unique characteristics and precursor origin. The cells can be found in vivo in Flt3L gene deleted (-/-) mice injected with recombinant M-CSF.

The mice were generated with the intention to elucidate in vivo DC developmental regions in steady state and inflammation in situ.

We found that the cooperation between IFNalpha,beta and Flt3L (FL) plays an important role in the defense against Herpes simplex virus type 1 (HSV-1) in neonates. Treatment of neonatal mice with recombinant IFNalpha has a short-term, FL-independent and a long-term, FL-dependent protective effect against HSV-1. In mice lacking FL, neonatal resistance against HSV-1 is very low and DC numbers in the spleen are reduced. The treatment of these mice with rIFNalpha at day 6 resulted in an increased resistance against infection with HSV-1 at day 7. In C57BL/6 mice, tr...

Hu-SCID mice were used to study responses to EBV and HIV.

The mice were infected with EBV and mount an immune response (i.e. cytotoxic T cell proliferation, some control of EBV driven B cell proliferation, perforine and granzyme expressing T cell infiltration in B cell infected areas in lymphoid organs in situ), however, specific T cells could not be detected directly ex vivo by looking at the most common EBV derived/presented epitopes (tetramer staining). Some animals developed EBV induced B cell lymphoproliferative disease.

These mice were infected with both CXCR4 as well as CCR5 tropic HIV-1 strains. HIV causes a disseminated infection and spreads in all newly generated lymphoid tissues, thus closely resembling HIV infection in humans. We are now aiming to improve the recipient mouse background by co-transplanting human mesenchymal stroma cells, and by adding human cytokines as well as human MHC. Furthermore, we use the mice to evaluate targeted therapies directed at human immune system cells as T cells, B cells, and dendritic cells.

We established “human hemato-lymphoid-system mice” by transplanting human CD34+ cord blood cells into irradiated newborn Rag2-/-gc-/- mice, leading to de novo development of human B, T, and dendritic cells.

IDO appears critical for the regulation of TNBS colitis upon CTLA-4 engagement, as the beneficial effect of anti-CTLA-4 treatment was lost in IDO-deficient mice. By contrast, the absence of IDO did not alter the course of inflammation in mice injected with TNBS only, an unexpected finding which suggests that IDO-dependent counter-regulation requires other factors/cells in addition to IDO production and T cell activation by TNBS.