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AssigneesThe Johns Hopkins University, The Brigham and Women's Hospital, Inc., T Cell Sciences, Inc.
InventorsDouglas T. Fearon, Lloyd B. Klickstein, Winnie W. Wong, Gerald R. Carson, Michael F. Concino, Stephen H. Ip, Savvas C. Makrides, Henry C. Marsh, Jr.
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The present invention relates to the C3b/C4b receptor (CR1) gene and its encoded protein. The invention also relates to CR1 nucleic acid sequences and fragments thereof comprising 70 nucleotides and their encoded peptides or proteins comprising 24 amino acids. The invention further provides for the expression of the CR1 protein and fragments thereof. The genes and proteins of the invention have uses in diagnosis and therapy of disorders involving complement activity, and various immune system or inflammatory disorders. In specific embodiments of the present invention detailed in the examples sections infra, the cloning, nucleotide sequence, and deduced amino acid sequence of a full-length CR1 cDNA and fragments thereof are described. The expression of the CR1 protein and fragments thereof is also described. Also described is the expression of a secreted CR1 molecule lacking a transmembrane region. The secreted CR1 molecule is shown to be useful in reducing damage caused by inflammation and in reducing myocardial infarct size and preventing reperfusion injury.
A method of treating a patient with a complement mediated immune disorder or a disorder which involves undesirable or inappropriate complement activity comprising administering to the patient a protein having an amino acid sequence as depicted in FIGS. 1A to 1P or a fragment thereof comprising at least two short consensus repeats and that has complement regulatory activity.
A method of treating a patient with a complement mediated immune disorder or a disorder which involves undesirable or inappropriate complement activity comprising administering to the patient a CR1 molecule comprising at least two short consensus repeats and that substantially lacks a transmembrane region and that has complement regulatory activity.
A method of treating or preventing damage in a patient caused by a myocardial infarct comprising administering to the patient a protein having an amino acid sequence as depicted in FIGS. 1A to 1P or a fragment thereof comprising at least two short consensus repeats and that has complement regulatory activity.
A method of treating or preventing damage in a patient caused by a myocardial infarct comprising administering to the patient a CR1 molecule comprising at least two short consensus repeats and that substantially lacks a transmembrane region and that has complement regulatory activity.
A method of treating or preventing damage in a patient caused by inflammation comprising administering to the patient a protein having an amino acid sequence as depicted in FIGS. 1A to 1P or a fragment thereof comprising at least two short consensus repeats and that has complement regulatory activity.
A method of treating or preventing damage in a patient caused by inflammation comprising administering to the patient a CR1 molecule comprising at least two short consensus repeats and that substantially lacks a transmembrane region and that has complement regulatory activity.
A method of treating a patient with a complement mediated immune disorder or a disorder which involves undesirable or inappropriate complement activity comprising administering to the patient a CR1 molecule that comprises LHR-A, LHR-B, LHR-C and LHR-D, and that substantially lacks a transmembrane region and a cytoplasmic region, and that has complement regulatory activity.
A method of treating or preventing damage in a patient caused by a myocardial infarct comprising administering to the patient a CR1 molecule that comprises LHR-A, LHR-B, LHR-C and LHR-D, and that substantially lacks a transmembrane region and a cytoplasmic region, and that has complement regulatory activity.
A method of treating or preventing damage in a patient caused by inflammation comprising administering to the patient a CR1 molecule that comprises LHR-A, LHR-B, LHR-C and LHR-D, and that substantially lacks a transmembrane region and a cytoplasmic region, and that has complement regulatory activity.
A method of treating a patient with a complement mediated immune disorder or a disorder which involves undesirable or inappropriate complement activity comprising administering to the patient a CR1 molecule that comprises LHR-B, LHR-C and LHR-D, and lacks LHR-A, and that substantially lacks a transmembrane region and a cytoplasmic region, and that has complement regulatory activity.
A method of treating or preventing damage in a patient caused by a myocardial infarct comprising administering to the patient a CR1 molecule that comprises LHR-B, LHR-C and LHR-D, and lacks LHR-A, and that substantially lacks a transmembrane region and a cytoplasmic intracellular region, and that has complement regulatory activity.
A method of treating or preventing damage in a patient caused by inflammation comprising administering to the patient a CR1 molecule that comprises LHR-B, LHR-C and LHR-D, and lacks LHR-A, and that substantially lacks a transmembrane region and a cytoplasmic region, and that has complement regulatory activity.
Dependencies are inferred from the claim text.