Novo Nordisk A/s

Innate Pharma S.a.s.

Centre National De La Recherche Scientifique

Novo Nordisk-a/s Novo Alle

University of Genoa

Innate Pharma

Inmate Pharma S.a.s.

Universita Di Genova

Stefan Zahn

Peter Andreas Nicolai Reumert Wagtmann

Anders Svensson

Kristian Kjaergaard

Søren Berg Padkær

Kristian Kjærgaard

Pieter Spee

Alessandro Moretta

Pascale Andre

Petrus Johannes Louis Spee

Mariella Della Chiesa

Ivan Svendsen

Laurent Gauthier

Francois Romagne

Birgitte Friedrichsen

Anker Jon Hansen

Soeren Lund

Elisabeth Douglas Galsgaard

Louise Hjerrild Zeuthen

Véronique Braud

Matthias Thorolfsson

Michael Wilken

Soren Berg Padkjaer

Francois Romagné

Milchael Wilken

Matthias Thórólfsson

Peter Reumert Wagtmann

Petrus Johannes Loius Spee

Laurant Gauthier

Pieter Johannes Louis Spee

Soren Berg Padkaer

François Romagne

Kristian KJÆRGAARD

Søren Lund

Søren Berg Padkaer

The present invention concerns human antibodies recognising the human C5a receptor. By binding to C5aR the antibodies inhibit C5a signalling, whereby the pro-inflammatory signal is inhibited. Based on the role of C5a and its receptor in stimulation of inflammation the invention further relates to therapeutic use of said human anti-C5aR antibodies and in particular in relation to treatment of immunological disorders.

Anti-C5a receptor antibodies

The present invention concerns human antibodies recognizing the human C5a receptor. By binding to C5aR the antibodies inhibit C5a signalling, whereby the pro-inflammatory signal is inhibited. Based on the role of C5a and its receptor in stimulation of inflammation the invention further relates to therapeutic use of said human anti-C5aR antibodies and in particular in relation to treatment of immunological disorders.

The present invention relates to agents and methods that are capable of augmenting NK-mediated killing of target cells by reducing inhibitory KIR signalling without reducing the binding of KIR to HLA-C. As described herein, transduction of negative signaling via KIR, upon binding of KIR to its HLA class I ligand, can involve a ligand-binding induced, conformational reorientation of the KIR molecules allowing interactions to form between adjacent KIRs in specific domains, leading to accelerated clustering. Methods and agents such as monoclonal antibodies for reducing KIR-mediated inhibition of NK cell cytotoxicity without reducing or blocking HLA-binding by, e.g., reducing or blocking dimerization of KIR, are provided.

KIR-binding agents and methods of use thereof

The present invention relates to monoclonal antibodies that are capable of specifically binding to lectin-like transcript 1 (LLT1), to polynucleotides encoding such antibodies, and to cells that express such antibodies. antibodies of the invention have utility in the treatment of autoimmune diseases and cancer, in which LLT1- and CD161-expressing cells play a role in disease pathogenesis.

LLT-1 antibodies with new functional properties

The present invention relates to monoclonal antibodies that are capable of specifically binding to lectin-like transcript 1 (LLT1), to polynucleotides encoding such antibodies and to cells that express such antibodies. Antibodies of the invention have utility in the treatment of autoimmune diseases and cancer, in which LLT1-and CD161-expressing cells play a role in disease pathogenesis.

Compositions and methods for regulating an immune response in a subject are described. More particularly, described are human antibodies that regulate the activity of NK cells and allow a potentiation of NK cell cytotoxicity in mammalian subjects, and antibodies having antigen-binding properties similar to those of human monoclonal antibody 1-7F9 or 1-4F1. Described also are also fragments and derivatives of such antibodies, as well as pharmaceutical compositions comprising the same and their uses, particularly for use in therapy, to increase NK cell activity or cytotoxicity in subjects.

Human anti-KIR antibodies

Nucleic acids encoding human anti-kir antibodies

The present invention relates to agents and methods that are capable of augmenting NK-mediated killing of target cells by reducing inhibitory KIR signalling without reducing the binding of KIR to HLA-C. As described herein, transduction of negative signaling via KIR, 5 upon binding of KIR to its HLA class I ligand, can involve a ligand-binding induced, conformational reorientation of the KIR molecules allowing interactions to form between adjacent KIRs in specific domains, leading to accelerated clustering. Methods and agents such as mono-clonal antibodies for reducing KIR-mediated inhibition of NK cell cytotoxicity without reducing or blocking HLA-binding by, e.g., reducing or blocking dimerization of KIR, are provided.

Growing community of inventors

Ballerup, Denmark

Stefan Zahn