Abstract: The present invention relates to the use of a compound that binds to a C-type lectin on the surface of a dendritic cell, in the preparation of a composition for modulating, in particular reducing, the immune response in an animal, in particular a human or another mammal. The composition in particular modulates the interactions between a dendritic cell and a T-cell, more specifically between a C-type lectin on the surface of a dendritic cell and an ICAM receptor on the surface of a T-cell. The compositions can be used for preventing/inhibiting immune responses to specific antigens, for inducing tolerance, for immunotherapy, for immunosuppression, for the treatment of autoimmune diseases, and the treatment of allergy. The compound that binds to a C-type lectin is preferably chosen from mannose, fucose, plant lectins, antibiotics, sugars, proteins or antibodies against C-type lectins. The invention also relates to such antibodies.

Abstract: The present invention relates to the use of a compound that binds to a C-type lectin on the surface of a dendritic cell, in the preparation of a composition for modulating, in particular reducing, the immune response in an animal, in particular a human or another mammal. The composition in particular modulates the interactions between a dendritic cell and a T-cell, more specifically between a C-type lectin on the surface of a dendritic cell and an ICAM receptor on the surface of a T-cell. The compositions can be used for preventing/inhibiting immune responses to specific antigens, for inducing tolerance, for immunotherapy, for immunosuppression, for the treatment of autoimmune diseases, and the treatment of allergy. The compound that binds to a C-type lectin is preferably chosen from mannose, fucose, plant lectins, antibiotics, sugars, proteins or antibodies against C-type lectins. The invention also relates to such antibodies.

Abstract: The C-type lectin DC-SIGN is absent in normal synovium but is highly expressed by CD68 positive macrophages in the synovium of rheumatoid arthritis patients. Accordingly, rheumatoid arthritis is diagnosed or treated by, respectively, assaying or blocking DC-SIGN. This can be accomplished by the use of agents, e.g., antibodies, which bind specifically to DCSIGN. Agents that bind to ICAM-3 are used to block inhibition of activation of macrophages by DC-SIGN-ICAM-3 interaction and cause inhibition of rheumatoid arthritis symptoms.

Abstract: Dendritic cells (DC) that express the type II C-type lectin DC-SIGN (CD209) are located in the submucosa of tissues, where they mediate HIV-1 entry. Interestingly, the pathogen Candida albicans, the major cause of hospital-acquired fungal infections, is found at similar sites. Here it is demonstrated that DC-SIGN is able to bind Candida albicans both in DC-SIGN transfected cell lines and in human monocyte derived DC. Moreover, in immature DC, DC-SIGN is able to internalize Candida in specific DC-SIGN enriched vesicles, distinct from those containing the mannose receptor (MR; CD206), which is another Candida receptor on DC. Together, these results demonstrate that C. albicans has two major receptors on human monocyte derived DC, these receptors being DC-SIGN and MR. Targeting of DC-SIGN offers novel opportunities to combat chronic forms of candidiasis.

Abstract: Dendritic cells (DC) that express the type II C-type lectin DC-SIGN (CD209) are located in the submucosa of tissues, where they mediate HIV-1 entry. Interestingly, the pathogen Candidaalbicans, the major cause of hospital-acquired fungal infections, is found at similar sites. Here it is demonstrated that DC-SIGN is able to bind Candida albicans both in DC-SIGN transfected cell lines and in human monocyte derived DC. Moreover, in immature DC, DC-SIGN is able to internalize Candida in specific DC-SIGN enriched vesicles, distinct from those containing the mannose receptor (MR; CD206), which is another Candida receptor on DC. Together, these results demonstrate that C. albicans has two major receptors on human monocyte derived DC, these receptors being DC-SIGN and MR. Targeting of DC-SIGN offers novel opportunities to combat chronic forms of candidiasis.

Abstract: The present invention relates to the use of a compound that binds to a C-type lectin on the surface of a dendritic cell, in the preparation of a composition for modulating, in particular reducing, the immune response in an animal, in particular a human or another mammal. The composition in particular modulates the interactions between a dendritic cell and a T-cell, more specifically between a C-type lectin on the surface of a dendritic cell and an ICAM receptor on the surface of a T-cell. The compositions can be used for preventing/inhibiting immune responses to specific antigens, for inducing tolerance, for immunotherapy, for immunosuppression, for the treatment of autoimmune diseases, and the treatment of allergy. The compound that binds to a C-type lectin is preferably chosen from mannose, fucose, plant lectins, antibiotics, sugars, proteins or antibodies against C-type lectins. The invention also relates to such antibodies.

Abstract: The present invention relates to the use of a compound that binds to a C-type lectin on the surface of a dendritic cell, in the preparation of a composition for modulating, in particular reducing, the immune response in an animal, in particular a human or another mammal. The composition in particular modulates the interactions between a dendritic cell and a T-cell, more specifically between a C-type lectin on the surface of a dendritic cell and an ICAM receptor on the surface of a T-cell. The compositions can be used for preventing/inhibiting immune responses to specific antigens, for inducing tolerance, for immunotherapy, for immunosuppression, for the treatment of autoimmune diseases, and the treatment of allergy. The compound that binds to a C-type lectin is preferably chosen from mannose, fucose, plant lectins, antibiotics, sugars, proteins or antibodies against C-type lectins. The invention also relates to such antibodies.

Abstract: The invention relates to the use of a compound that binds to a C-type lectin on the surface of a sinusoid endothelial layer, in the preparation of a composition for modulating, in particular reducing, the immune response in animal, in particular a human or another mammal. The sinusoid endothelial layer may be either constituted by liver sinusoid endothelial cells (LSEC) or by the lymph node sinusoidal zone.

Abstract: The present invention relates to the use of a compound that binds to a C-type lectin on the surface of a dendritic cell, in the preparation of a composition for modulating, in particular reducing, the immune response in an animal, in particular a human or another mammal. The composition in particular modulates the interactions between a dendritic cell and a T-cell, more specifically between a C-type lectin on the surface of a dendritic cell and an ICAM receptor on the surface of a T-cell. The compositions can be used for preventing/inhibiting immune responses to specific antigens, for inducing tolerance, for immunotherapy, for immunosuppression, for the treatment of auto-immune diseases, the treatment of allergy, and/or for inhibiting HIV infection. The compound that binds to a C-type lectin is preferably chosen from mannose, fucose, plant lectins, antibiotics, sugars, proteins or antibodies against C-type lectins.

Abstract: Dendritic cells (DC) that express the type II C-type lectin DC-SIGN (CD209) are located in the submucosa of tissues, where they mediate HIV-1 entry. Interestingly, the pathogen Candidaalbicans, the major cause of hospital-acquired fungal infections, is found at similar sites. Here it is demonstrated that DC-SIGN is able to bind Candida albicans both in DC-SIGN transfected cell lines and in human monocyte derived DC. Moreover, in immature DC, DC-SIGN is able to internalize Candida in specific DC-SIGN enriched vesicles, distinct from those containing the mannose receptor (MR; CD206), which is another Candida receptor on DC. Together, these results demonstrate that C. albicans has two major receptors on human monocyte derived DC, these receptors being DC-SIGN and MR. Targeting of DC-SIGN offers novel opportunities to combat chronic forms of candidiasis.

Abstract: The C-type lectin DC-SIGN is absent in normal synovium but is highly expressed by CD68 positive macrophages in the synovium of rheumatoid arthritis patients. Accordingly, rheumatoid arthritis is diagnosed or treated by, respectively, assaying or blocking DC-SIGN. This can be accomplished by the use of agents, e.g., antibodies, which bind specifically to DCSIGN. Agents that bind to ICAM-3 are used to block inhibition of activation of macrophages by DC-SIGN-ICAM-3 interaction and cause inhibition of rheumatoid arthritis symptoms.

Abstract: The present invention relates to the use of a compound that binds to a C-type lectin on the surface of a dendritic cell, in the preparation of a composition for modulating, in particular reducing, the immune response in an animal, in particular a human or another mammal. The composition in particular modulates the interactions between a dendritic cell and a T-cell, more specifically between a C-type lectin on the surface of a dendritic cell and an ICAM receptor on the surface of a T-cell. The compositions can be used for preventing/inhibiting immune responses to specific antigens, for inducing tolerance, for immunotherapy, for immunosuppression, for the treatment of autoimmune diseases, and the treatment of allergy. The compound that binds to a C-type lectin is preferably chosen from mannose, fucose, plant lectins, antibiotics, sugars, proteins or antibodies against C-type lectins. The invention also relates to such antibodies.

Abstract: The present invention relates to the use of a compound that binds to a C-type lectin on the surface of a dendritic cell, in the preparation of a composition for modulating, in particular reducing, the immune response in an animal, in particular a human or another mammal. The composition in particular modulates the interactions between a dendritic cell and a T-cell, more specifically between a C-type lectin on the surface of a dendritic cell and an ICAM receptor on the surface of a T-cell. The compositions can be used for preventing/inhibiting immune responses to specific antigens, for inducing tolerance, for immunotherapy, for immunosuppression, for the treatment of autoimmune diseases, and the treatment of allergy. The compound that binds to a C-type lectin is preferably chosen from mannose, fucose, plant lectins, antibiotics, sugars, proteins or antibodies against C-type lectins. The invention also relates to such antibodies.

Abstract: The invention relates to the use of a compound that binds to a C-type lectin on the surface of a sinusoid endothelial layer, in the preparation of a composition for modulating, in particular reducing, the immune response in animal, in particular a human or another mammal. The sinusoid endothelial layer may be either constituted by liver sinusoid endothelial cells (LSEC) or by the lymph node sinusoidal zone.