Abstract: The invention is in the field of therapy of antibody deficiencies. Inventors demonstrate for the first time in both controls and IgA-deficient patients. systemic anti-microbiota IgG responses correlate with reduced inflammation suggesting that systemic IgG responses contribute to the gut microbiota confinement. Furthermore. SIgAd-associated inflammation is inversely correlated with systemic anti-commensal IgG responses, which may thus serve as a second line of defense. Altogether, these data suggest that systemic IgG and intestinal IgA cooperate in different body compartments to limit systemic pro-inflammatory pathways. As selective IgA deficient patients harbour elevated seric anti-commensal IgG levels. these findings suggest that in selective IgA deficiency, microbiota confinement is obtained at the price of a strong inflammatory response. Accordingly. the invention relates to a composition containing immunoglobulins A (IgA). more particularly secretory IgA.

Abstract: The invention is in the field of therapy of antibody deficiencies. Inventors demonstrate for the first time in both controls and IgA-deficient patients. systemic anti-microbiota IgG responses correlate with reduced inflammation suggesting that systemic IgG responses contribute to the gut microbiota confinement. Furthermore. SIgAd-associated inflammation is inversely correlated with systemic anti-commensal IgG responses, which may thus serve as a second line of defense. Altogether, these data suggest that systemic IgG and intestinal IgA cooperate in different body compartments to limit systemic pro-inflammatory pathways. As selective IgA deficient patients harbour elevated seric anti-commensal IgG levels. these findings suggest that in selective IgA deficiency, microbiota confinement is obtained at the price of a strong inflammatory response. Accordingly. the invention relates to a composition containing immunoglobulins A (IgA). more particularly secretory IgA.

Abstract: The invention is in the field of therapy of antibody deficiencies. Inventors demonstrate for the first time in both controls and IgA-deficient patients, systemic anti-microbiota IgG responses correlate with reduced inflammation suggesting that systemic IgG responses contribute to the gut microbiota confinement. Furthermore, SIgAd-associated inflammation is inversely correlated with systemic anti-commensal IgG responses, which may thus serve as a second line of defense. Altogether, these data suggest that systemic IgG and intestinal IgA cooperate in different body compartments to limit systemic pro-inflammatory pathways. As selective IgA deficient patients harbour elevated seric anti-commensal IgG levels, these findings suggest that in selective IgA deficiency, microbiota confinement is obtained at the price of a strong inflammatory response.

Abstract: The invention is in the field of therapy of antibody deficiencies. Inventors demonstrate for the first time in both controls and IgA-deficient patients, systemic anti-microbiota IgG responses correlate with reduced inflammation suggesting that systemic IgG responses contribute to the gut microbiota confinement. Furthermore, SIgAd-associated inflammation is inversely correlated with systemic anti-commensal IgG responses, which may thus serve as a second line of defense. Altogether, these data suggest that systemic IgG and intestinal IgA cooperate in different body compartments to limit systemic pro-inflammatory pathways. As selective IgA deficient patients harbour elevated seric anti-commensal IgG levels, these findings suggest that in selective IgA deficiency, microbiota confinement is obtained at the price of a strong inflammatory response.

Abstract: The invention is in the field of therapy of antibody deficiencies such as immune diseases and inflammatory disorders. The inventors demonstrate for the first time the convergence of intestinal IgA and serum IgG responses toward the same microbial targets, under homeostatic conditions. Private anti-microbiota IgG specificities are induced in IgA-deficient patients, but are not found in IgG pools from healthy donors, partially explaining why substitutive IgG (IVIG) cannot regulate antibody deficiency-associated gut dysbiosis and intestinal translocation. Finally, in both controls and IgA-deficient patients, systemic anti-microbiota IgG responses correlate with reduced inflammation suggesting that systemic IgG responses contribute to the gut microbiota confinement.

Abstract: The present invention relates to methods and kits for identifying effector regulatory T cells. In particular the present invention relates to use of CD15s as a biomarker for eTreg cells. The present invention also relates to a method for identifying effector Treg cells (eTreg) in a fluid sample comprising the steps of i) detecting the cell surface expression of CD4, CD25, CD127 and CD15s markers on the cell population contained in the fluid sample and ii) concluding that the cells expressing CD4, CD25, CD127 at low levels and CD15s are the effector Treg cells. The present invention also relates to a method for identifying effector Treg cells (eTreg) in a tissue sample comprising the steps of i) detecting the cell expression of CD4, CD25, Foxp3 and CD15s markers and ii) concluding that the cells expressing CD4, CD25, Foxp3 and CD15s are the effector Treg cells.

Abstract: The present invention relates to methods and kits for identifying effector regulatory T cells. In particular the present invention relates to use of CD15s as a biomarker for eTreg cells. The present invention also relates to a method for identifying effector Treg cells (eTreg) in a fluid sample comprising the steps of i) detecting the cell surface expression of CD4, CD25, CD127 and CD15s markers on the cell population contained in the fluid sample and ii) concluding that the cells expressing CD4, CD25, CD127 at low levels and CD15s are the effector Treg cells. The present invention also relates to a method for identifying effector Treg cells (eTreg) in a tissue sample comprising the steps of i) detecting the cell expression of CD4, CD25, Foxp3 and CD15s markers and ii) concluding that the cells expressing CD4, CD25, Foxp3 and CD15s are the effector Treg cells.

Abstract: The present invention relates to methods and kits for identifying effector regulatory T cells. In particular the present invention relates to use of CD15s as a biomarker for eTreg cells. The present invention also relates to a method for identifying effector Treg cells (eTreg) in a fluid sample comprising the steps of i) detecting the cell surface expression of CD4, CD25, CD127 and CD15s markers on the cell population contained in the fluid sample and ii) concluding that the cells expressing CD4, CD25, CD127 at low levels and CD15s are the effector Treg cells. The present invention also relates to a method for identifying effector Treg cells (eTreg) in a tissue sample comprising the steps of i) detecting the cell expression of CD4, CD25, Foxp3 and CD15s markers and ii) concluding that the cells expressing CD4, CD25, Foxp3 and CD15s are the effector Treg cells.

Abstract: The present invention concerns modulators of the CX3CR1 receptor. More specifically, antagonists and agonists of the CX3CR1 receptor have been identified. These antagonists and agonists can be used for treating an inflammatory disorder, an autoimmune disorder, a cardiovascular disease, a neurodegenerative disease, a graft versus host disease, a behavioral disorder, a cicatrisation disorder, a viral infection, cancer or pain. They may also be used as an adjuvant in a vaccine composition.

Abstract: The present invention provides a method for the design and/or the selection of agonist or antagonist chemokine variants combining a phage display technology and a screening on living cells expressing the receptor of the corresponding native chemokine. It also provides RANTES variants having agonist properties towards said receptor, and methods for preventing and/or curing viral diseases, as well as clues for preventing and/or curing inflammatory or malignant diseases.

Abstract: The present invention provides a method for the design and/or the selection of agonist or antagonist chemokine variants combining a phage display technology and a screening on living cells expressing the receptor of the corresponding native chemokine. It also provides RANTES variants having agonist properties towards said receptor, and methods for preventing and/or curing viral diseases, as well as clues for preventing and/or curing inflammatory or malignant diseases.

Abstract: The present invention provides a method for the design and/or the selection of agonist or antagonist chemokine variants combining a phage display technology and a screening on living cells expressing the receptor of the corresponding native chemokine. It also provides RANTES variants having agonist properties towards said receptor, and methods for preventing and/or curing viral diseases, as well as clues for preventing and/or curing inflammatory or malignant diseases.

Abstract: The present invention provides a method for the design and/or the selection of agonist or antagonist chemokine variants combining a phage display technology and a screening on living cells expressing the receptor of the corresponding native chemokine. It also provides RANTES variants having agonist properties towards said receptor, and methods for preventing and/or curing viral diseases, as well as clues for preventing and/or curing inflammatory or malignant diseases.

Abstract: The present invention provides a method for the design and/or the selection of agonist or antagonist chemokine variants combining a phage display technology and a screening on living cells expressing the receptor of the corresponding native chemokine. It also provides RANTES variants having agonist properties towards said receptor, and methods for preventing and/or curing viral deseases.

Abstract: Disclosed is a method of treating a heterogeneous population of cells to link together copies of two or more nucleic acid sequences from at least some of the cells, the arrangement being such that copies of the DNA sequences from an individual cell are preferentially linked in the vicinity of the nucleic acid from which the copies are derived. Also disclosed are recombinant proteins expressed by the method of the invention and kits for performing said method.