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...

Antigen-specific CD4+ T cells were followed in these immunized individuals using generated peptide-MHC class II multimers.

Anti-tumor responses were followed in melanoma patients that were vaccinated with autologous DCs loaded with a combination of tumor Ag peptides.

These constructs were prepared for a per-clinical model of breast cancer.

The normal donors were studied for effector vs. memory T cell responses.

DCs with blocked beta-glucan, mannan and chitin receptors were exposed to these fungi.

The effect of environmental factors on development of high affinity CTL was investigated using a system whereby OT-1 cells were primed in vitro by engineered APC. After a 20 h priming phase, CTL were transferred to recipient mice that were either naïve, or had been injected with activated dendritic cells one day earlier, thus creating a reactive lymph node.

A recombinant Leishmania major parasite expressing a fluorescent tracer was used for the infection of BALB/c (H2-d) mice. This was done to investigate whether infected DC process pathogen-derived antigen and stimulate antigen-specific CD4+ T cells in vivo.

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

The animal(s) were immunized in vivo with in vitro matured DC and / or treated using a maturation signal.

A significant number of patients was enrolled in the DC-based immunotherapy trial. After vaccination, vaccine-induced depigmentation and vitiligo were observed.

4 metastatic melanoma patients were actively vaccinated and additional injections were performed in disease free patients, in patients with stable disease or with slowly progressive disease.

By immunizing mice with ovalbumin-conjugated anti-Siglec-H Ab in the presence of CpG, we demonstrated generation of antigen-specific CD8 T cells in vivo.

The patients were vaccinated with a vaccine composed by autologous DCs pulsed with apoptotic allogenic prostate carcinoma cell line LNCap.

These patients receive a DC vaccine composed by autologous DCs electroporated with mRNA encoding CD40L, CD70, caTLR4 and one tumorantigen (gp100, Tyrosinase, Mage-C2 or Mage-A3).

These patients are involved in a phase II clinical trial for melanoma and are treated with OncoVexGMCSF. Data so far indicates that OncoVex can destroy both injected and un-injected melanoma deposits. The trial is still in progress.

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 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.

These mice were treated with intact anti-CTLA-4 antibodies. This induced the development of regulatory T cells expressing high levels of ICOS and producing IL-10. These regulatory T cells inhibit Th1 responses, in vitro and in vivo, and repress experimental intestinal inflammation, by a mechanism involving IL-10 and IDO.