Abstract: According to the present invention, a composition for inducing or activating dendritic cell-like cells so as to treat or prevent cancer by immunotherapy is provided. Specifically, the following is provided: an agent for activating cancer immunity, which comprises, as an active ingredient, the following REIC protein: (a) a protein consisting of the amino acid sequence shown in SEQ ID NO: 2; or (b) a protein consisting of an amino acid sequence derived from the amino acid sequence shown in SEQ ID NO: 2 by substitution, deletion, or addition of one or more amino acid(s) and having the activity of inducing differentiation from monocytes into dendritic cell-like cells.

Abstract: The invention provides CD4+CD25? T cells and Tr1-like regulatory T cells (i.e., contact-independent Type 1-like regulatory T cells), processes for their production and their use for regulatory purposes.

Abstract: Described herein are methods of cancer immunotherapy, particularly methods of preparing a population of enhanced dendritic cells and methods of treating cancer using the enhanced dendritic cells.

Abstract: Isolated monoclonal antibodies which bind to human DEC-205 and related antibody-based compositions and molecules are disclosed. Also disclosed are pharmaceutical compositions comprising the antibodies, as well as therapeutic and diagnostic methods for using the antibodies.

Abstract: The present invention is a method for preventing or treating an immune-relevant disease by modulating commensal microbiota populations via antibiotics, exogenous microbiota and/or probiotics.

Abstract: The invention relates to the regulation of the immune system, and in particular to the finding that the CLEC9a molecule is a marker for dendritic cells which are capable of cross-presenting extracellular antigens via the MHC class I pathway. This makes them particularly suitable for generation of cytotoxic T lymphocyte responses. Materials and methods are provided both for the induction of immune responses against target antigens, and for the inhibition or suppression of undesirable immune responses in which these cells are involved.

Abstract: The invention relates to a method for producing ready to use, antigen loaded or unloaded, cryoconserved mature dendritic cells especially for the production of a vaccine containing said dendritic cells, wherein immature dendritic cells are cultivated in the presence of suitable maturation stimuli and the mature dendritic cells thus obtained are frozen. The dendritic cells can be loaded with antigen before freezing. The invention also relates to a vaccine which can be obtained according to the inventive method and to a composition containing frozen, mature dendritic cells which are loaded with antigen.

Abstract: A method for generating/expanding in vitro a CD4+CD25+ T regulatory (Tr) cell and the use thereof in the treatment of diseases associated with a cell-mediated immune response (including T- and antibody-mediated responses).

Abstract: This invention relates to culture-expanded T suppressor cells derived from CD25?CD4+ T cells, and their use in modulating immune responses. This invention provides methods of producing culture-expanded T suppressor cells, which are antigen specific, and their use in modulating autoimmune diseases and transplantation rejection.

Abstract: The invention involves the discovery that if dendritic cells loaded with a tumor antigen are cultured in interleukin-15 (IL-15), or if T cells activated by the dendritic cells are cultured in IL-15, Treg activity that is specific for the tumor antigen is reduced. This reduction in Treg activity results in an increase in anti-tumor immune response. Another embodiment of the invention involves the discovery that incubating dendritic cells with a MAP kinase inhibitor in combination with IL-15 gives synergistic benefits when the dendritic cells are used to activate T cells. Dendritic cell and T cell compositions incubated with IL-15 or a MAP kinase inhibitor are provided.

Abstract: The present invention is related to Preprocalcitonin antigen T epitopes, presented by the Major Histocompatibility Complex I (MHC I). These peptides can be used in cancer immunotherapy.

Abstract: The present invention includes compositions and methods for targeting the LOX-1 receptor on immune cells and uses for the anti-LOX-1 antibodies.

Abstract: With the current invention, we provide new methods of enhancing the T-cell stimulatory capacity of human dendritic cells (DCs) and their use in cancer vaccination. The method comprises the introduction of different molecular adjuvants to human DCs through transfection with at least two mRNA or DNA molecules encoding markers selected from the group of: CD40L, CD70, constitutively active TLR4 (caTLR4), IL-12p70, EL-selectin, CCR7 and/or 4-1 BBL; or in combination with inhibition of SOCS, A20, PD-L1 and/or STAT3 expression, for example through siRNA transfection. We could show a clear increase in the immunostimulatory capacity of DCs obtained in this way, enabling them to elicit an unexpectedly high T-cell immune response in vitro.

Abstract: An antibody binding to IPC was obtained by using an animal cell in which a cell membrane protein associatable with ILT7 was co-expressed as an immunogen. The antibody of the invention has a high specificity which allows immunological distinction between other ILT family molecules and ILT7. The anti-ILT7 antibody of the invention bound to IPC and inhibited the activity thereof. With the anti-ILT7 antibody of the invention, the IPC activity can be inhibited and an interferon-related disease can be treated or prevented. ILT7 expression is maintained even in IPC in the presence of IFN?. Therefore, an inhibitory action of IPC activity by the anti-ILT7 antibody can be expected even in an autoimmune disease patient with an increased production of IFN?.

Abstract: The present invention relates to biological and medical applications of an anti-CD160 monoclonal antibody (CL1-R2 CNCM I-3204) and of the conservative equivalents thereof. It more particularly relates to the applications of these anti-CD160 compounds in the fields of EC angiogenesis, and NK and T cytokine production.

Abstract: A method of inducing dendritic cell (DC) development by administering Macrophage-Colony Stimulating Factor (M-CSF) is provided. M-CSF induces DCs to differentiate into Subtypes, for example plasmacytoid DCs and conventional DCs. Said differentiation is independent of Fms-like-Tyrosine-Kinase 3-Ligand (FL) and/or Granulocyte-Macrophage-Colony Stimulating Factor (GM-CSF). Induction with M-CSF can be achieved in vitro from hematopoietic precursors, such as bone marrow cells, or in vivo. In vitro, M-CSF-derived DCs can be used to produce cytokines and to stimulate other immune response cells. M-CSF can also be used to induce precursor cells removed from an animal to develop into DCs. In addition, these isolated DCs can be exposed to antigens to stimulate a specific immune response when reintroduced into the animal. Treatments for Cancers, such as Acute Myeloid Leukemia, and autoimmune diseases such as Systemic Lupus Erythematosus, are also provided in the invention.

Abstract: The present invention relates to methods and compositions for the treatment and diagnosis of immune disorders, especially T helper lymphocyte-related disorders. In particular, the invention describes a gene known in the art, alternatively, as ST2, T1 and Fit-1, and referred to herein as the 103 gene. The 103 gene is disclosed herein to be differentially expressed in TH2 cells and not in TH1 cells. Further, the 103 gene product is demonstrated herein to be an important modulator of TH2 and TH2-like immune response both in vitro and in vivo. Thus, the 103 gene, its gene products and antibodies that specifically bind thereto can be used diagnostically or as targets for therapeutic intervention in the treatment of a variety of immune disorders. In this regard, the invention provides methods for the identification and therapeutic use of compounds for treatments of immune disorders, especially TH cell subpopulation-related disorders and including TH2 and TH2-like disorders (i.e.

Abstract: A complex comprising at least one heat shock protein (HSP) and at least one peptide selected from the group consisting of R1-QXRAA-R2 with R1=peptide with 1-10 amino acids R2=peptide with 1-10 amino acids X=K or R GFFYTPK (insulin 23-29) SEQ ID No 1 GFFYTPKT (insulin 23-30) SEQ ID No 2 IYPPNANK (DER p1) SEQ ID No 3 GIEYIQHNGVVQESYYR (DER P1) SEQ ID No 4 ASTTTNYT (gp120 of HIV) SEQ ID No 5 DYEYLINVIHAFQYV (PLP 56-70) SEQ ID No 6 EKLIETYFSKNYQDYEYLINVI (PLP 43-64) SEQ ID No 7 KTTICGKGLSATVT (PLP 104-117) SEQ ID No 8 HSLGKWLGHPDKF (PLP 139-151 C140 ô S140) SEQ ID No 9 PRHPIRVELPCRISP (MOG 8-22) SEQ ID No 10 DEGGYTCFFRDHSYQ (MOG 92-106) SEQ ID No 11 Ac-ASQKRPSQRHG (MBP ac1-11) SEQ ID No 12 TGILDSIGRFFSG (MBP 35-47) SEQ ID No 13 VHFFKNIVTPRTP (MBP 89-101) SEQ ID No 14 HCLGKWLGHPDKF (PLP 139-151) SEQ ID No 15 MEVGWYRSPFSRVVHLYRNGK (MOG) SEQ ID No 16 QKRAAYDQYGHAAFE (E. Coli DnaJ) SEQ ID No. 17 QKRAAVDTYCRHNYG (HLA DRB1*0401) SEQ ID No. 18 QRRAAYDQYGHAAFE SEQ ID No. 19 and QRRAAVDTYCRHNYG SEQ ID No. 20.

Abstract: The present invention comprises compositions and methods for making monoclonal antibodies. The present invention further comprises vectors that replicate the immune system components, particularly an antigen-presenting cell (APC) element of the immune synapse. Additionally, the present invention may further comprise synthetic T-cells.

Abstract: The present invention relates to the identification of proteins located on the cell surface of dendritic cells or precursors thereof, particularly antigen presenting dendritic cells. In particular, the present invention relates to compounds such as antibodies that bind these proteins. These compounds can be used to detect and/or enrich a subset of dendritic cells or precursors thereof. These compounds can also be used to target antigens to dendritic cells or precursors thereof to modulate a humoral and/or T cell mediated immune response to an antigen, or used to target cytotoxic agents to dendritic cells or precursors thereof involved in diseased states.