Depletion of activated macrophages with a folate receptor-beta-specific antibody improves symptoms in mouse models of rheumatoid arthritis
Objectives Most therapies for autoimmune and inflammatory diseases either neutralize or suppress production of inflammatory cytokines produced by activated macrophages (e.g., TNFα, IL-1, IL-6, IL-17, GM-CSF). However, no approved therapies directly target this activated subset of macrophages. Method...
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| Vydáno v: | Arthritis research & therapy Ročník 21; číslo 1; s. 143 - 14 |
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| Hlavní autoři: | , , , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
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London
BioMed Central
07.06.2019
BioMed Central Ltd Springer Nature B.V BMC |
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| ISSN: | 1478-6362, 1478-6354, 1478-6362 |
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| Abstract | Objectives
Most therapies for autoimmune and inflammatory diseases either neutralize or suppress production of inflammatory cytokines produced by activated macrophages (e.g., TNFα, IL-1, IL-6, IL-17, GM-CSF). However, no approved therapies directly target this activated subset of macrophages.
Methods
First, we undertook to examine whether the folate receptor beta (FR-β) positive subpopulation of macrophages, which marks the inflammatory subset in animal models of rheumatoid arthritis, might constitute the prominent population of macrophages in inflamed lesions in humans. Next, we utilized anti-FR-β monoclonal antibodies capable of mediating antibody-dependent cell cytotoxicity (ADCC) to treat animal models of rheumatoid arthritis and peritonitis.
Results
Human tissue samples of rheumatoid arthritis, Crohn’s disease, ulcerative colitis, idiopathic pulmonary fibrosis, nonspecific interstitial pneumonia, chronic obstructive pulmonary disease, systemic lupus erythematosus, psoriasis, and scleroderma are all characterized by dramatic accumulation of macrophages that express FR-β, a protein not expressed on resting macrophages or any other healthy tissues. A monoclonal antibody to FR-β accumulates specifically in inflamed lesions of murine inflammatory disease models and successfully treats such models of rheumatoid arthritis and peritonitis. More importantly, elimination of FR-β-positive macrophages upon treatment with an anti-FR-β monoclonal antibody promotes the departure of other immune cells, including T cells, B cells, neutrophils, and dendritic cells from the inflamed lesions.
Conclusions
These data suggest that specific elimination of FR-β-expressing macrophages may constitute a highly specific therapy for multiple autoimmune and inflammatory diseases and that a recently developed human anti-human FR-β monoclonal antibody (m909) might contribute to suppression of this subpopulation of macrophages. |
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| AbstractList | Objectives Most therapies for autoimmune and inflammatory diseases either neutralize or suppress production of inflammatory cytokines produced by activated macrophages (e.g., TNFα, IL-1, IL-6, IL-17, GM-CSF). However, no approved therapies directly target this activated subset of macrophages. Methods First, we undertook to examine whether the folate receptor beta (FR-β) positive subpopulation of macrophages, which marks the inflammatory subset in animal models of rheumatoid arthritis, might constitute the prominent population of macrophages in inflamed lesions in humans. Next, we utilized anti-FR-β monoclonal antibodies capable of mediating antibody-dependent cell cytotoxicity (ADCC) to treat animal models of rheumatoid arthritis and peritonitis. Results Human tissue samples of rheumatoid arthritis, Crohn’s disease, ulcerative colitis, idiopathic pulmonary fibrosis, nonspecific interstitial pneumonia, chronic obstructive pulmonary disease, systemic lupus erythematosus, psoriasis, and scleroderma are all characterized by dramatic accumulation of macrophages that express FR-β, a protein not expressed on resting macrophages or any other healthy tissues. A monoclonal antibody to FR-β accumulates specifically in inflamed lesions of murine inflammatory disease models and successfully treats such models of rheumatoid arthritis and peritonitis. More importantly, elimination of FR-β-positive macrophages upon treatment with an anti-FR-β monoclonal antibody promotes the departure of other immune cells, including T cells, B cells, neutrophils, and dendritic cells from the inflamed lesions. Conclusions These data suggest that specific elimination of FR-β-expressing macrophages may constitute a highly specific therapy for multiple autoimmune and inflammatory diseases and that a recently developed human anti-human FR-β monoclonal antibody (m909) might contribute to suppression of this subpopulation of macrophages. Most therapies for autoimmune and inflammatory diseases either neutralize or suppress production of inflammatory cytokines produced by activated macrophages (e.g., TNFα, IL-1, IL-6, IL-17, GM-CSF). However, no approved therapies directly target this activated subset of macrophages.OBJECTIVESMost therapies for autoimmune and inflammatory diseases either neutralize or suppress production of inflammatory cytokines produced by activated macrophages (e.g., TNFα, IL-1, IL-6, IL-17, GM-CSF). However, no approved therapies directly target this activated subset of macrophages.First, we undertook to examine whether the folate receptor beta (FR-β) positive subpopulation of macrophages, which marks the inflammatory subset in animal models of rheumatoid arthritis, might constitute the prominent population of macrophages in inflamed lesions in humans. Next, we utilized anti-FR-β monoclonal antibodies capable of mediating antibody-dependent cell cytotoxicity (ADCC) to treat animal models of rheumatoid arthritis and peritonitis.METHODSFirst, we undertook to examine whether the folate receptor beta (FR-β) positive subpopulation of macrophages, which marks the inflammatory subset in animal models of rheumatoid arthritis, might constitute the prominent population of macrophages in inflamed lesions in humans. Next, we utilized anti-FR-β monoclonal antibodies capable of mediating antibody-dependent cell cytotoxicity (ADCC) to treat animal models of rheumatoid arthritis and peritonitis.Human tissue samples of rheumatoid arthritis, Crohn's disease, ulcerative colitis, idiopathic pulmonary fibrosis, nonspecific interstitial pneumonia, chronic obstructive pulmonary disease, systemic lupus erythematosus, psoriasis, and scleroderma are all characterized by dramatic accumulation of macrophages that express FR-β, a protein not expressed on resting macrophages or any other healthy tissues. A monoclonal antibody to FR-β accumulates specifically in inflamed lesions of murine inflammatory disease models and successfully treats such models of rheumatoid arthritis and peritonitis. More importantly, elimination of FR-β-positive macrophages upon treatment with an anti-FR-β monoclonal antibody promotes the departure of other immune cells, including T cells, B cells, neutrophils, and dendritic cells from the inflamed lesions.RESULTSHuman tissue samples of rheumatoid arthritis, Crohn's disease, ulcerative colitis, idiopathic pulmonary fibrosis, nonspecific interstitial pneumonia, chronic obstructive pulmonary disease, systemic lupus erythematosus, psoriasis, and scleroderma are all characterized by dramatic accumulation of macrophages that express FR-β, a protein not expressed on resting macrophages or any other healthy tissues. A monoclonal antibody to FR-β accumulates specifically in inflamed lesions of murine inflammatory disease models and successfully treats such models of rheumatoid arthritis and peritonitis. More importantly, elimination of FR-β-positive macrophages upon treatment with an anti-FR-β monoclonal antibody promotes the departure of other immune cells, including T cells, B cells, neutrophils, and dendritic cells from the inflamed lesions.These data suggest that specific elimination of FR-β-expressing macrophages may constitute a highly specific therapy for multiple autoimmune and inflammatory diseases and that a recently developed human anti-human FR-β monoclonal antibody (m909) might contribute to suppression of this subpopulation of macrophages.CONCLUSIONSThese data suggest that specific elimination of FR-β-expressing macrophages may constitute a highly specific therapy for multiple autoimmune and inflammatory diseases and that a recently developed human anti-human FR-β monoclonal antibody (m909) might contribute to suppression of this subpopulation of macrophages. Most therapies for autoimmune and inflammatory diseases either neutralize or suppress production of inflammatory cytokines produced by activated macrophages (e.g., TNFα, IL-1, IL-6, IL-17, GM-CSF). However, no approved therapies directly target this activated subset of macrophages. First, we undertook to examine whether the folate receptor beta (FR-β) positive subpopulation of macrophages, which marks the inflammatory subset in animal models of rheumatoid arthritis, might constitute the prominent population of macrophages in inflamed lesions in humans. Next, we utilized anti-FR-β monoclonal antibodies capable of mediating antibody-dependent cell cytotoxicity (ADCC) to treat animal models of rheumatoid arthritis and peritonitis. Human tissue samples of rheumatoid arthritis, Crohn's disease, ulcerative colitis, idiopathic pulmonary fibrosis, nonspecific interstitial pneumonia, chronic obstructive pulmonary disease, systemic lupus erythematosus, psoriasis, and scleroderma are all characterized by dramatic accumulation of macrophages that express FR-β, a protein not expressed on resting macrophages or any other healthy tissues. A monoclonal antibody to FR-β accumulates specifically in inflamed lesions of murine inflammatory disease models and successfully treats such models of rheumatoid arthritis and peritonitis. More importantly, elimination of FR-β-positive macrophages upon treatment with an anti-FR-β monoclonal antibody promotes the departure of other immune cells, including T cells, B cells, neutrophils, and dendritic cells from the inflamed lesions. These data suggest that specific elimination of FR-β-expressing macrophages may constitute a highly specific therapy for multiple autoimmune and inflammatory diseases and that a recently developed human anti-human FR-β monoclonal antibody (m909) might contribute to suppression of this subpopulation of macrophages. Abstract Objectives Most therapies for autoimmune and inflammatory diseases either neutralize or suppress production of inflammatory cytokines produced by activated macrophages (e.g., TNFα, IL-1, IL-6, IL-17, GM-CSF). However, no approved therapies directly target this activated subset of macrophages. Methods First, we undertook to examine whether the folate receptor beta (FR-β) positive subpopulation of macrophages, which marks the inflammatory subset in animal models of rheumatoid arthritis, might constitute the prominent population of macrophages in inflamed lesions in humans. Next, we utilized anti-FR-β monoclonal antibodies capable of mediating antibody-dependent cell cytotoxicity (ADCC) to treat animal models of rheumatoid arthritis and peritonitis. Results Human tissue samples of rheumatoid arthritis, Crohn’s disease, ulcerative colitis, idiopathic pulmonary fibrosis, nonspecific interstitial pneumonia, chronic obstructive pulmonary disease, systemic lupus erythematosus, psoriasis, and scleroderma are all characterized by dramatic accumulation of macrophages that express FR-β, a protein not expressed on resting macrophages or any other healthy tissues. A monoclonal antibody to FR-β accumulates specifically in inflamed lesions of murine inflammatory disease models and successfully treats such models of rheumatoid arthritis and peritonitis. More importantly, elimination of FR-β-positive macrophages upon treatment with an anti-FR-β monoclonal antibody promotes the departure of other immune cells, including T cells, B cells, neutrophils, and dendritic cells from the inflamed lesions. Conclusions These data suggest that specific elimination of FR-β-expressing macrophages may constitute a highly specific therapy for multiple autoimmune and inflammatory diseases and that a recently developed human anti-human FR-β monoclonal antibody (m909) might contribute to suppression of this subpopulation of macrophages. Objectives Most therapies for autoimmune and inflammatory diseases either neutralize or suppress production of inflammatory cytokines produced by activated macrophages (e.g., TNFα, IL-1, IL-6, IL-17, GM-CSF). However, no approved therapies directly target this activated subset of macrophages. Methods First, we undertook to examine whether the folate receptor beta (FR-β) positive subpopulation of macrophages, which marks the inflammatory subset in animal models of rheumatoid arthritis, might constitute the prominent population of macrophages in inflamed lesions in humans. Next, we utilized anti-FR-β monoclonal antibodies capable of mediating antibody-dependent cell cytotoxicity (ADCC) to treat animal models of rheumatoid arthritis and peritonitis. Results Human tissue samples of rheumatoid arthritis, Crohn’s disease, ulcerative colitis, idiopathic pulmonary fibrosis, nonspecific interstitial pneumonia, chronic obstructive pulmonary disease, systemic lupus erythematosus, psoriasis, and scleroderma are all characterized by dramatic accumulation of macrophages that express FR-β, a protein not expressed on resting macrophages or any other healthy tissues. A monoclonal antibody to FR-β accumulates specifically in inflamed lesions of murine inflammatory disease models and successfully treats such models of rheumatoid arthritis and peritonitis. More importantly, elimination of FR-β-positive macrophages upon treatment with an anti-FR-β monoclonal antibody promotes the departure of other immune cells, including T cells, B cells, neutrophils, and dendritic cells from the inflamed lesions. Conclusions These data suggest that specific elimination of FR-β-expressing macrophages may constitute a highly specific therapy for multiple autoimmune and inflammatory diseases and that a recently developed human anti-human FR-β monoclonal antibody (m909) might contribute to suppression of this subpopulation of macrophages. Objectives Most therapies for autoimmune and inflammatory diseases either neutralize or suppress production of inflammatory cytokines produced by activated macrophages (e.g., TNF[alpha], IL-1, IL-6, IL-17, GM-CSF). However, no approved therapies directly target this activated subset of macrophages. Methods First, we undertook to examine whether the folate receptor beta (FR-[beta]) positive subpopulation of macrophages, which marks the inflammatory subset in animal models of rheumatoid arthritis, might constitute the prominent population of macrophages in inflamed lesions in humans. Next, we utilized anti-FR-[beta] monoclonal antibodies capable of mediating antibody-dependent cell cytotoxicity (ADCC) to treat animal models of rheumatoid arthritis and peritonitis. Results Human tissue samples of rheumatoid arthritis, Crohn's disease, ulcerative colitis, idiopathic pulmonary fibrosis, nonspecific interstitial pneumonia, chronic obstructive pulmonary disease, systemic lupus erythematosus, psoriasis, and scleroderma are all characterized by dramatic accumulation of macrophages that express FR-[beta], a protein not expressed on resting macrophages or any other healthy tissues. A monoclonal antibody to FR-[beta] accumulates specifically in inflamed lesions of murine inflammatory disease models and successfully treats such models of rheumatoid arthritis and peritonitis. More importantly, elimination of FR-[beta]-positive macrophages upon treatment with an anti-FR-[beta] monoclonal antibody promotes the departure of other immune cells, including T cells, B cells, neutrophils, and dendritic cells from the inflamed lesions. Conclusions These data suggest that specific elimination of FR-[beta]-expressing macrophages may constitute a highly specific therapy for multiple autoimmune and inflammatory diseases and that a recently developed human anti-human FR-[beta] monoclonal antibody (m909) might contribute to suppression of this subpopulation of macrophages. Keywords: Folate receptor beta, Activated macrophages, Inflammatory disease, Autoimmune disease, Rheumatoid arthritis Most therapies for autoimmune and inflammatory diseases either neutralize or suppress production of inflammatory cytokines produced by activated macrophages (e.g., TNF[alpha], IL-1, IL-6, IL-17, GM-CSF). However, no approved therapies directly target this activated subset of macrophages. First, we undertook to examine whether the folate receptor beta (FR-[beta]) positive subpopulation of macrophages, which marks the inflammatory subset in animal models of rheumatoid arthritis, might constitute the prominent population of macrophages in inflamed lesions in humans. Next, we utilized anti-FR-[beta] monoclonal antibodies capable of mediating antibody-dependent cell cytotoxicity (ADCC) to treat animal models of rheumatoid arthritis and peritonitis. Human tissue samples of rheumatoid arthritis, Crohn's disease, ulcerative colitis, idiopathic pulmonary fibrosis, nonspecific interstitial pneumonia, chronic obstructive pulmonary disease, systemic lupus erythematosus, psoriasis, and scleroderma are all characterized by dramatic accumulation of macrophages that express FR-[beta], a protein not expressed on resting macrophages or any other healthy tissues. A monoclonal antibody to FR-[beta] accumulates specifically in inflamed lesions of murine inflammatory disease models and successfully treats such models of rheumatoid arthritis and peritonitis. More importantly, elimination of FR-[beta]-positive macrophages upon treatment with an anti-FR-[beta] monoclonal antibody promotes the departure of other immune cells, including T cells, B cells, neutrophils, and dendritic cells from the inflamed lesions. These data suggest that specific elimination of FR-[beta]-expressing macrophages may constitute a highly specific therapy for multiple autoimmune and inflammatory diseases and that a recently developed human anti-human FR-[beta] monoclonal antibody (m909) might contribute to suppression of this subpopulation of macrophages. |
| ArticleNumber | 143 |
| Audience | Academic |
| Author | Low, Stewart A. Wang, Bingbing Ruppert, Clemens Dimitrov, Dimiter S. Niessen, Hans W. M. Oliver, Stephen J. Feng, Yang Matteson, Eric L. Putt, Karson S. Hu, Yingwen Shen, Jiayin Murphy, Linda Nickerson-Nutter, Cheryl Low, Philip S. Jansen, Gerrit |
| Author_xml | – sequence: 1 givenname: Yingwen surname: Hu fullname: Hu, Yingwen organization: Department of Chemistry, Purdue University – sequence: 2 givenname: Bingbing surname: Wang fullname: Wang, Bingbing organization: Department of Chemistry, Purdue University – sequence: 3 givenname: Jiayin surname: Shen fullname: Shen, Jiayin organization: Department of Chemistry, Purdue University – sequence: 4 givenname: Stewart A. surname: Low fullname: Low, Stewart A. organization: Department of Chemistry, Purdue University – sequence: 5 givenname: Karson S. surname: Putt fullname: Putt, Karson S. organization: Institute for Drug Discovery, Purdue University – sequence: 6 givenname: Hans W. M. surname: Niessen fullname: Niessen, Hans W. M. organization: Department of Pathology and Cardiac Surgery, ACS, Amsterdam UMC – sequence: 7 givenname: Eric L. surname: Matteson fullname: Matteson, Eric L. organization: Division of Rheumatology, and Department of Health Sciences Research, Mayo Clinic – sequence: 8 givenname: Linda surname: Murphy fullname: Murphy, Linda organization: Department of Biochemistry and Molecular Biology, Mayo Clinic College of Medicine – sequence: 9 givenname: Clemens surname: Ruppert fullname: Ruppert, Clemens organization: Justus-Liebig University Giessen, Department of Internal Medicine, Biomedizinisches Forschungszentrum Seltersberg – sequence: 10 givenname: Gerrit surname: Jansen fullname: Jansen, Gerrit organization: Department of Rheumatology, Amsterdam Rheumatology and Immunology Center, VU University Medical Center – sequence: 11 givenname: Stephen J. surname: Oliver fullname: Oliver, Stephen J. organization: Department of Medicine, New York University School of Medicine – sequence: 12 givenname: Yang surname: Feng fullname: Feng, Yang organization: Protein Interactions Section, Laboratory of Experimental Immunology, Cancer and Inflammation Program, Center for Cancer, National Cancer Institute-Frederick, National Institutes of Health – sequence: 13 givenname: Dimiter S. surname: Dimitrov fullname: Dimitrov, Dimiter S. organization: Center for Antibody Therapeutics, University of Pittsburgh – sequence: 14 givenname: Cheryl surname: Nickerson-Nutter fullname: Nickerson-Nutter, Cheryl organization: HuLow Medical – sequence: 15 givenname: Philip S. surname: Low fullname: Low, Philip S. email: plow@purdue.edu organization: Department of Chemistry, Purdue University, Institute for Drug Discovery, Purdue University |
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| Keywords | Autoimmune disease Activated macrophages Rheumatoid arthritis Folate receptor beta Inflammatory disease |
| Language | English |
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| PublicationTitle | Arthritis research & therapy |
| PublicationTitleAbbrev | Arthritis Res Ther |
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Most therapies for autoimmune and inflammatory diseases either neutralize or suppress production of inflammatory cytokines produced by activated... Most therapies for autoimmune and inflammatory diseases either neutralize or suppress production of inflammatory cytokines produced by activated macrophages... Objectives Most therapies for autoimmune and inflammatory diseases either neutralize or suppress production of inflammatory cytokines produced by activated... Abstract Objectives Most therapies for autoimmune and inflammatory diseases either neutralize or suppress production of inflammatory cytokines produced by... |
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| SubjectTerms | Activated macrophages Adalimumab Anakinra Animals Antibodies Antibodies, Monoclonal - therapeutic use Arthritis Arthritis, Rheumatoid - drug therapy Arthritis, Rheumatoid - immunology Arthritis, Rheumatoid - pathology Autoimmune disease Autoimmune diseases B cells Binding proteins Canakinumab Care and treatment Cells, Cultured Chronic obstructive lung disease Chronic obstructive pulmonary disease Colitis Crohn's disease Cytokines Cytokines - metabolism Cytotoxicity Dendritic cells Disease Disease Models, Animal Ethanol Fibrosis Folate Receptor 2 - immunology Folate receptor beta Folic acid Golimumab Granulocytes Health aspects Humans Immunity, Cellular Inflammation Inflammatory bowel disease Inflammatory disease Inflammatory diseases Lupus Lupus erythematosus Macrophage Activation Macrophages Macrophages - immunology Macrophages - metabolism Macrophages - pathology Medicine Medicine & Public Health Mice Monoclonal antibodies Neutrophils Orthopedics Peritonitis Physiological aspects Pneumonia Psoriasis Pulmonary fibrosis Research Article Rheumatoid arthritis Rheumatoid factor Rheumatology Rilonacept Scleroderma Scleroderma (Disease) Systemic lupus erythematosus T cells Tocilizumab Tumor necrosis factor Ulcerative colitis Ustekinumab Vitamin B |
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| Title | Depletion of activated macrophages with a folate receptor-beta-specific antibody improves symptoms in mouse models of rheumatoid arthritis |
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