Abstract: The invention is based on the discovery that interleukin-1 alpha (IL-1alpha) is expressed on the proinflammatory CD14+CD16+ monocyte subset. Importantly, since IL-1alpha appears to be almost exclusively expressed on this monocyte subset and not other leukocytes, it represents an ideal marker for targeting the CD14+CD16+ monocyte subset. The effectiveness of an agent that depletes such pathogenic cells or modulates IL-1alpha function on such cells type can be monitored by assessing CD14+CD16+ monocyte levels or functionality.
Abstract: Fully human monoclonal Abs includes (i) an antigen-binding variable region that exhibits very high binding affinity for IL-1? and (ii) a constant region that is effective at both activating the complement system though C1q binding and binding to several different Fc receptors.
Abstract: Methods of detecting individuals at risk for atherosclerosis and related vascular diseases involving the detection of IL-1? autoantibodies, as well as therapeutic methods to prevent or treat atherosclerosis and related vascular disease by administering a pharmaceutical composition comprising IL-1? autoantibodies.
Abstract: Immunization of a mammal with IL-1?, which causes the mammal to generate IL-1? autoantibodies, can be used to reduce the risk and severity of, or to reduce progression of, an atherosclerosis-related disease in the mammal. Progression of atherosclerosis-related diseases such as peripheral ischemic heart disease, coronary artery disease, cerebrovascular disease, and peripheral arterial disease can be reduced using this treatment.
Abstract: Methods, compositions, and kits relating to selecting a prophylactic or therapeutic antibody less likely to induce or aggravate an anti-antibody response in a subject administered the antibody. An antibody for administration to a subject may be selected to match, or at least more closely resemble, the allotypic phenotype of the subject's endogenous antibodies.
Abstract: Methods, compositions, and kits relating to selecting a prophylactic or therapeutic antibody less likely to induce or aggravate an anti-antibody response in a subject administered the antibody. An antibody for administration to a subject may be selected to match, or at least more closely resemble, the allotypic phenotype of the subject's endogenous antibodies.
Abstract: Fully human monoclonal Abs includes (i) an antigen-binding variable region that exhibits very high binding affinity for IL-1? and (ii) a constant region that is effective at both activating the complement system though C1q binding and binding to several different Fc receptors.
Abstract: Fully human monoclonal Abs includes (i) an antigen-binding variable region that exhibits very high binding affinity for IL-1? and (ii) a constant region that is effective at both activating the complement system though C1q binding and binding to several different Fc receptors.
Abstract: Fully human monoclonal Abs includes (i) an antigen-binding variable region that exhibits very high binding affinity for IL-1? and (ii) a constant region that is effective at both activating the complement system though C1q binding and binding to several different Fc receptors.
Abstract: Fully human monoclonal Abs includes (i) an antigen-binding variable region that exhibits very high binding affinity for IL-1? and (ii) a constant region that is effective at both activating the complement system though C1q binding and binding to several different Fc receptors.
Abstract: Administration of a monoclonal Ab (mAb) that specifically targets IL-1? is useful to treating articular and extra-articular symptoms of arthritis.
Abstract: Fully human monoclonal Abs includes (i) an antigen-binding variable region that exhibits very high binding affinity for IL-1? and (ii) a constant region that is effective at both activating the complement system though C1q binding and binding to several different Fc receptors.
Abstract: Methods, compositions, and kits relating to selecting a prophylactic or therapeutic antibody less likely to induce or aggravate an anti-antibody response in a subject administered the antibody. An antibody for administration to a subject may be selected to match, or at least more closely resemble, the allotypic phenotype of the subject's endogenous antibodies.
Abstract: Methods, compositions, and kits relating to selecting a prophylactic or therapeutic antibody less likely to induce or aggravate an anti-antibody response in a subject administered the antibody. An antibody for administration to a subject may be selected to match, or at least more closely resemble, the allotypic phenotype of the subject's endogenous antibodies.
Abstract: Methods, compositions, and kits relating to selecting a prophylactic or therapeutic antibody less likely to induce or aggravate an anti-antibody response in a subject administered the antibody. An antibody for administration to a subject may be selected to match, or at least more closely resemble, the allotypic phenotype of the subject's endogenous antibodies.
Abstract: Methods, compositions, and kits relating to selecting a prophylactic or therapeutic antibody less likely to induce or aggravate an anti-antibody response in a subject administered the antibody. An antibody for administration to a subject may be selected to match, or at least more closely resemble, the allotypic phenotype of the subject's endogenous antibodies.
Abstract: Immunization of a mammal with IL-1?, which causes the mammal to generate IL-1? autoantibodies, can be used to reduce the risk and severity of, or to reduce progression of, an atherosclerosis-related disease in the mammal. Progression of atherosclerosis-related diseases such as peripheral ischemic heart disease, coronary artery disease, cerebrovascular disease, and peripheral arterial disease can be reduced using this treatment.
Abstract: The invention is based on the discovery that interleukin-1 alpha (IL-1alpha) is expressed on the proinflammatory CD14+CD16+ monocyte subset. Importantly, since IL-1alpha appears to be almost exclusively expressed on this monocyte subset and not other leukocytes, it represents an ideal marker for targeting the CD14+CD16+ monocyte subset. The effectiveness of an agent that depletes such pathogenic cells or modulates IL-1alpha function on such cells type can be monitored by assessing CD14+CD16+ monocyte levels or functionality.