Abstract: A method for choosing a patient to anti-CLEVER-1 therapy prior to beginning anti-CLEVER-1 therapy using one or several of the inflammatory markers selected from interferon gamma (IFN?), tumour necrosis factor alpha (TNF-?), interleukin 6 (IL-6), interleukin 8 (IL-8) and C-reactive protein. When the measured level of the inflammatory marker is substantially within the reference values of the inflammatory marker or lower than the average reference value of the inflammatory marker, it is an indication to choose the patient and begin the anti-CLEVER-1 therapy.

Abstract: The invention relates to stable formulations comprising an anti-CLEVER-1 antibody or antigen binding fragment(s) thereof, a buffer and a stabilizing agent. The present invention further relates to stable formulations of an anti-CLEVER-1 antibody or antigen binding fragments thereof for use in treatment of various diseases and disorders.

Abstract: Use of an agent capable of inhibiting CLEVER-1 expression or binding to CLEVER-1 in combination with an inhibitor of interleukin and/or the respective receptor, and optionally further with an agent capable of binding to interferon-alpha/beta receptor (IFNAR) in a treatment of diseases.

Abstract: A vascular adhesion protein-1 (VAP-1) inhibitor can be used as a regulator of reactive oxygen species (ROS) concentration in ex vivo culturing of hematopoietic stem cells, which enables a method of producing an expanded population of hematopoietic5 stem cells ex vivo. Further, a VAP-1 inhibitor can be used in the treatment of bone marrow suppression or bone barrow failure in an individual.

Abstract: A method for monitoring a patient's response to anti-Clever-1 therapy and estimating the need for combination therapy based on the expression levels of one or more cell surface marker selected from PD-1, PD-L1, CTLA-4, ICOS, OX40, 41BB, LAG3, TIM3, CD28, CD25 and CXCR3 on leucocytes in relation to anti-Clever-1 treatment and choosing the best combination agent to initiate treatment together with anti-Clever-1 therapy after observed changes in one or more cell surface marker expression.

Abstract: A method for determining a potency of a therapeutic anti-Clever-1 antibody or fragment(s) thereof capable of binding to human Clever-1 by inhibition of a modified low-density lipoprotein uptake, wherein the inhibition of modified low-density lipoprotein uptake is an indication of biological activity of said anti-Clever-1 antibody or fragment(s) thereof.

Abstract: A method for determining a patient's responsiveness to a therapy comprising administration of type I interferon in order to make the decision to treat a patient with type I interferon and use of a SNP rs9984273 (C/T) in IFNAR2 as a marker for determining a patient's responsiveness to said therapy.

Abstract: A method for preventing and/or treating systemic inflammatory response syndrome (SIRS), the method comprising administration of an agent capable of up-regulating CD73 in combination with a glucocorticoid and/or an agent capable of agonizing the glucocorticoid receptor, wherein an agent capable of up-regulating CD73 and a glucocorticoid and/or an agent capable of agonizing the glucocorticoid receptor are administered sequentially. An agent capable of up-regulating CD73 is administered prior to a glucocorticoid and/or an agent capable of agonizing the glucocorticoid receptor.

Abstract: Altering levels of soluble CLEVER-1 in circulation achieves either immune activation or immune-suppression of T cells in an individual. Soluble CLEVER-1 has been found to bind to activated T cells using Receptor of Activated Protein C Kinase 1 (RACK1) as its ligand.

Abstract: The invention relates to use of TLR9 antagonist in a method for treating cancer and/or chronic infection by downregulating Clever-1 expression on alternatively activated immunosuppressive macrophages.

Abstract: This invention relates to an agent and a humanized antibody or single chain Fv or Fab fragment capable of binding to human CLEVER-1 recognizing an epitope of CLEVER-1, wherein the epitope is discontinuous and comprises the sequences: PFTVLVPSVSSFSSR and QEITVTFNQFTK. This invention relates also an agent capable of binding to an epitope of human CLEVER-1 for use in removing tumour or antigen induced immunosuppression. Further, the invention relates to a pharmaceutical composition comprising the agent capable of binding to human CLEVER-1 and an appropriate excipient.

Abstract: The invention relates to an agent capable of binding to CLEVER-1 in combination with PD-1 and/or PD-L inhibitor for use in a treatment of cancer.

Abstract: This invention relates to an agent and a humanized antibody or single chain Fv or Fab fragment capable of binding to human CLEVER-1 recognizing an epitope of CLEVER-1, wherein the epitope is discontinuous and comprises the sequences: PFTVLVPSVSSFSSR and QEITVTFNQFTK. This invention relates also an agent capable of binding to an epitope of human CLEVER-1 for use in removing tumour or antigen induced immunosuppression. Further, the invention relates to a pharmaceutical composition comprising the agent capable of binding to human CLEVER-1 and an appropriate excipient.

Abstract: A method of determining the efficacy of anti-Clever-1 therapy by measuring lysosomal pH, and a method of increasing lysosomal pH for improving an activation of the immune system in a patient, in which method an agent that inhibiting Clever-1 on the lysosomal proton pump (vATPase) is administered to a patient.

Abstract: An agent capable of binding to CLEVER-1 in an individual can be used in activating macrophages to switch their phenotype from M2 macrophages into M1 macrophages. The invention relates to methods for utilizing the macrophages ability to switch their phenotype. In one aspect, the invention relates to a method for estimating of the efficacy of anti-CLEVER-1 therapy by monitoring a modulation of M2 macrophages into M1 macrophages, when an agent capable of binding to CLEVER-1 is administered in a patient, wherein an increased TNF-alpha secretion or HLA-DR expression is indicative of modulation of M2 macrophages into M1 macrophages.

Abstract: A method for determining a patient's responsiveness to a therapy comprising administration of type I interferon in order to make the decision to treat a patient with type I interferon and use of a SNP rs9984273 (C/T) in IFNAR2 as a marker for determining a patient's responsiveness to said therapy.

Abstract: The invention relates to a novel cell derived from the human body, where said cell comprises a Clever-1 receptor; to a method for affecting the immune system of an individual and for treatment of diseases or conditions related to the function of the immune system and to methods for screening of cancer patients that may respond to an anti-Clever-1 therapy or for diagnosing of a pregnancy complication or for estimating the risk of such complication in a pregnant woman.

Abstract: This invention relates to an agent and a humanized antibody or single chain Fv or Fab fragment capable of binding to human CLEVER-1 recognizing an epitope of CLEVER-1, wherein the epitope is discontinuous and comprises the sequences: PFTVLVPSVSSFSSR and QEITVTFNQFTK. This invention relates also an agent capable of binding to an epitope of human CLEVER-1 for use in removing tumour or antigen induced immunosuppression. Further, the invention relates to a pharmaceutical composition comprising the agent capable of binding to human CLEVER-1 and an appropriate excipient.

Abstract: A pharmaceutical formulation in a lyophilised form, which comprises pharmacologically effective amount of interferon beta-1a as an active ingredient, disaccharides as a bulking agent and a non-ionic surfactant. After reconstitution, the composition can be administered intravenously.

Abstract: This invention concerns methods for monitoring the development of and for treatment of ARDS in a patient. The method for monitoring the development of ARDS is based on comparing the level or activity of the biomarkers obtained in a sample drawn at a later point of time to the levels or activities of the same biomarkers in a sample drawn at a previous point of time. A favorable change in the level or activity of a certain biomarker represents a regression of the disease (recovery of the patient), and, conversely, an adverse change in the level or activity of a certain biomarker represents a worsening of the disease. If, for example, the level or activity for one or more of the biomarkers monitored discontinues to show a favorable change or starts to show an unfavorable change, the treatment of the patient is enhanced by administering a therapeutically active agent useful in the treatment of ARDS.