1935 results about "Macrophage cell" patented technology

This invention is directed to the field of medical implants, and more specifically to biodegradable injectable implants and their methods of manufacture and use. The injectable implants disclosed herein comprise glycolic acid and bio-compatible/bio-absorbable polymeric particles containing a polymer of lactic acid. The particles are small enough to be injected through a needle but large enough to avoid engulfment by macrophages. The injectables of this invention may be in a pre-activated solid form or an activated form (e.g., injectable suspension or emulsion).

A method and system for treating a patient to repair damaged tissue which includes exposing a selected area of bone marrow of a patient to ultrasound waves or ultra shock waves so that cells comprising stem cells, progenitor cells or macrophages are generated in the area of the bone marrow of the patient due to the ultrasound, converting the cells from the bone marrow of the patient and reducing the damaged tissue in the bone marrow of the patient by repairing the damaged tissue.

The present invention is based on the discovery that proteins produced in insect cell cultures are glycosylated in a unique manner that causes them to be selectively imported by cells that express mannose receptors on their membranes, particularly macrophages. Proteins that are selectively imported into cells containing mannose receptors are provided, as well as pharmaceutical compositions containing such proteins and methods for producing such proteins. Application of the present invention to produce proteins useful for treating lysosomal storage disorders is also disclosed. Engineering of cells to express mannose receptors so that they will selectively import proteins produced in insect cells is also taught, as well as a protein targeting system using such cells and proteins. Finally, an improved elution buffer for the purification of proteins produced in insect cells from a Concanavalin A column is provided.

An objective of the present invention is to provide a therapeutic agent for treating rheumatoid arthritis, juvenile rheumatoid arthritis, macrophage activation syndrome, septicemia, and FR-β expressing leukemia, which induces apoptosis in activated macrophages and folate receptor beta (FR-β) expressing leukemia cells to specifically destroy these cells. An FR-β monoclonal antibody of the present invention is preferably an IgG-type monoclonal antibody which specifically reacts with a human-type FR-β antigen and is produced from a clone resulting from immunization with an FR-β expressing B300-19 cell. The FR-β monoclonal antibody of the present invention specifically reacts with the FR-β antigen of activated macrophages and FR-β expressing leukemia cells and a therapeutic agent of the present invention contains an FR-β antibody immunotoxin which causes apoptosis in activated macrophages and FR-β expressing leukemia cells, as an active ingredient. Further, suitable administration form for the therapeutic agent of the present invention includes intravenous injection as well as joint injection in the case of therapeutic agents for rheumatoid arthritis and juvenile arthritis.

An apparatus and method according to the present invention can be provided, e.g., for a cell specific laser therapy of atherosclerotic plaques, particularly to systems and methods for targeting endogenous light absorbers present within plaque macrophages and exogenous nanoparticle targeting. In one exemplary embodiment, an electro-magnetic radiation can be forwarded to an anatomical structure. The electromagnetic radiation may have at least one property configured to (a) modify at least one characteristic of at least one first cell, and (b) minimize any modification of and/or modify at least one characteristic of at least second cell. The first and second cells may be different from one another, the characteristics of the first and second cells can be different from one another, and the first cell and/or the second cell may have at least one macrophage feature, and the characteristic of the at least one first cell and/or the at least one second cell can be temperature. According to still another exemplary embodiment, a location associated with the first cell and the second cell can be determined. For example, the electromagnetic radiation can be forwarded in a vicinity of the location.

Inhibitors of MIF having a naphthyridine backbone are provided which have utility in the treatment of a variety of disorders, including the treatment of pathological conditions associated with MIF activity. The inhibitors of MIF have the following structures:

including stereoisomers, prodrugs and pharmaceutically acceptable salts thereof, wherein n, R, R₁, R₂, X, Y and Z are as defined herein. Compositions containing an inhibitor of MIF in combination with a pharmaceutically acceptable carrier are also provided, as well as methods for use of the same.

The invention provides a human antibody that binds human CSF-1R with high affinity. Antibodies of the present invention have significant advantages over the antibodies known in the art by being multifunctional: inhibiting signaling of CSF-1R, internalizing and inducing CSF-1R degradation and stimulating ADCC in cell including tumors, macrophages and monocytes. They are also shown to be effective in treating leukemia, breast, endometrial and prostate cancer alone or in combination with docetaxel, paclitaxel, Herceptin® or doxorubicin.

Detectably labeled macrophage scavenger receptor antagonists useful for the diagnosis and monitoring of various cardiovascular diseases including but not limited to atherosclerosis, vulnerable plaque, coronary artery disease, renal disease, thrombosis, transient ischemia due to clotting, stroke, myocardial infarction, organ transplant, organ failure and hypercholesterolemia.

The invention provides a chimeric antigen receptor (CAR) (a) an antigen binding domain of HN1 or SS, a transmembrane domain, and an intracellular T cell signaling domain, or (b) an antigen binding domain of SS1, a transmembrane domain, an intracellular T cell signaling domain, and a granulocyte-macrophage colony-stimulating factor (GM-CSF) receptor 2 leader. Nucleic acids, recombinant expression vectors, host cells, populations of cells, antibodies, or antigen binding portions thereof, and pharmaceutical compositions relating to the CARs are disclosed. Methods of detecting the presence of cancer in a mammal and methods of treating or preventing cancer in a mammal are also disclosed.

This invention provides: agents determined to be capable of specifically inhibiting the fusion of a macrophage-tropic primary isolate of HIV-1 to a CD4⁺ cell, but not a T cell-tropic isolate of HIV-1 to a CD4⁺ cell; and agents determined to be capable of specifically inhibiting the fusion of a T cell-tropic isolate of HIV-1 to a CD4⁺ cell, but not a macrophage-tropic primary isolate of HIV-1 to a CD4⁺ cell. This invention also provides: agents capable of specifically inhibiting the fusion of a macrophage tropic primary isolate of HIV-1 with a CD+ cell susceptible to infection by a macrophage-tropic primary isolate of HIV-1; and agents capable of specifically inhibiting the fusion of a T cell-tropic isolate of HIV-1 with a CD4⁺ cell susceptible to infection by a T cell-tropic isolate of HIV-1. The agents include but are not limited to antibodies. This invention further provides: methods of inhibiting fusion of a macrophage-tropic primary isolate of HIV-1 with a CD+ cell susceptible to infection by a macrophage-tropic primary isolate of HIV-1 which comprises contacting the CD4⁺ cell with an amount of an agent capable of specifically inhibiting such fusion so as to thereby inhibit such fusion; and methods of inhibiting fusion of a T cell-tropic isolate of HIV-1 with a CD4⁺ cell susceptible to infection by a T cell-tropic isolate of HIV-1 which comprises contacting the CD4⁺ cell with an amount of an agent capable of specifically inhibiting such fusion so as to thereby inhibit such fusion.

Novel activating receptors of the Ig super-family expressed on human myeloid cells, called TREM(s) (triggering receptor expressed on myeloid cells) are provided. Specifically, two (2) members of TREMs, TREM-1 and TREM-2 are disclosed. TREM-1 is a transmembrane glycoprotein expressed selectively on blood neutrophils and a subset of monocytes but not on lymphocytes and other cell types and is upregulated by bacterial and fungal products. Use of TREM-1 in treatment and diagnosis of various inflammatory diseases is also provided. TREM-2 is also a transmembrane glycoprotein expressed selectively on mast cells and peripheral dendritic cells (DCs) but not on granulocytes or monocytes. DC stimulation via TREM-2 leads to DC maturation and resistance to apoptosis, and induces strong upregulation of CCR⁷ and subsequent chemotaxis toward macrophage inflammatory protein 3-β. TREM-2 has utility in modulating host immune responses in various immune disorders, including autoimmune diseases and allergic disorders.

The invention relates to the field of protein, and specifically relates to a milk-derived bioactive polypeptide LPLP with in-vitro antioxidant activity and immunity improving function. An amino acid sequence of the polypeptide is Leu-Pro-Leu-Pro. In-vitro anti-oxidation and in-vitro immune function promotion experiments prove that the polypeptide LPLP has good anti-oxidation bioactivity and cellular immunity promotion activity. With the polypeptide LPLP, free radicals in bodies can be removed, such that harm of the free radicals to human bodies can be reduced; and the bioactive polypeptide LPLP can enhance macrophage phagocytic function, can improve body capacity for resisting external pathogens, can reduce body incidence rate, and does not cause body immunological rejection. The polypeptide has important significance in developing dairy products, health products and medicines with anti-oxidation function and immunity enhancing function.

The present invention relates to a method for predicting the risk of a subject developing a cardiovascular event comprising detecting at least one biomarker in (a sample of) the cardiovascular system from said subject, wherein said biomarker comprises at least one protein selected from the group consisting of Tumor Necrosis Factor Alpha Precursor; Lysosomal-associated Membrane Protein (1); Interleukin-5 Precursor; Interleukin-6 Precursor; C-C Motif Chemokine (2) Precursor; C-C Motif Chemokine (5) Precursor RANTES; Cathepsin L1 Precursor; Adenylate Kinase (1); Leukotriene B4 Receptor (1); Complement Factor D; Secreted Phosphoprotein (1); Small Inducible Cytokine A17 Precursor; C-X-C Motif Chemokine (10) Precursor; Tumor Necrosis Factor Ligand Superfamily Member (11)(RANKL); C-C Motif Chemokine (18) Precursor; 72 kDa Type IVCollagenase Precursor; Neutrophil Collagenase Precursor; fatty acid binding protein (4); calpain (2), (m/II) large subunit; Macrophage Migration Inhibitory Factor; Cathepsin S Precursor; Interleukin (13) Precursor; and soluble ICAM-1.

The invention discloses rhodococcus ruber and application of same as an immunologic adjuvant in preparing vaccine. The rhodococcus ruber is also called rhodococcus ruber RDC-01, and the preservation number is CGMCC (China General Microbiological Culture Collection Center) NO. 16640. The rhodococcus ruber disclosed by the invention has the function of increasing and regulating the body immunity andis capable of nonspecifically enhancing the activity of TB (Tuberculosis) lymphocyte, macrophagocyte and NK cells and inducing multiple cell factors such as interferon, and the rhodococcus ruber canbe used as the immunologic adjuvant after being inactivated so as to be added in an oil-adjuvant inactive vaccine, so that generation of an animal antibody induced by the vaccine can be obviously promoted; compared with single use of the oil-adjuvant inactive vaccine, a high-titre antibody can be generated, the use is safe, long-term and short-term toxic and side effects are not generated, and anapplication prospect in the field of preparation of vaccines for animals is good.

The present invention relates to a method for stimulating wound healing, and more particularly to a method for stimulating wound healing in a subject in need thereof, comprising administering to a wound of the subject an effective amount for stimulating wound healing of a composition, wherein the composition comprises p43 having an amino acid sequence set forth in SEQ ID NO: 1 or functional equivalents thereof. The composition used in the method of the present invention can be efficiently utilized for the wound healing, since p43, an effective ingredient of the composition, has an excellent effect on the wound healing by its action including the induction of macrophage/monocyte and endothelial cell, re-epithelization, proliferation of fibroblasts or angiogenesis.