Novel molecular targets for systemic lupus erythematosus (509 views)
Curr Drug Targets (ISSN: 1389-4501), 2002 Jun; 3(3): 223-228.
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Paper type: Journal Article,
Impact factor: 3.597, 5-year impact factor: 3.558
Url: http://www.scopus.com/inward/record.url?eid=2-s2.0-0036001051&partnerID=40&md5=f20fb6aa35c6d58abf643f305ae56dcf
Keywords: Antiidiotypic Antibody, Antiinflammatory Agent, Antimalarial Agent, Azathioprine, Cd16 Antigen, Chymotrypsin, Complement, Corticosteroid, Cyclophosphamide, Cyclosporin, Fc Receptor, Glucocorticoid, Immunoglobulin G, Immunosuppressive Agent, Methotrexate, Monoclonal Antibody, Pepsin A, Tetramer, Tg 19320, Tripeptide Derivative, Unclassified Drug, Oligopeptide, Acquired Immune Deficiency Syndrome, Animal Experiment, Animal Model, Antigen Antibody Complex, Autoimmune Disease, Cataract, Combinatorial Chemistry, Controlled Study, Depression, Disease Predisposition, Drug Bioavailability, Drug Blood Level, Drug Efficacy, Drug Formulation, Drug Half Life, Drug Mechanism, Drug Stability, Drug Synthesis, Drug Targeting, Drug Urine Level, Effector Cell, Female, Glomerulonephritis, Human, In Vivo Study, Infection, Inflammation, Insomnia, Kidney Injury, Microbial Immunity, Molecular Interaction, Mouse, Mouse Strain, Multiple Myeloma, Nausea And Vomiting, Nonhuman, Osteoporosis, Pathogenesis, Review, Rheumatoid Arthritis, Systemic Lupus Erythematosus, Tissue Injury, Validation Process, Weight Gain, Metabolism, Pathophysiology,
Affiliations:
*** IBB - CNR ***
XEPTAGEN S.p.A, Via A. Olivetti 1, Pozzuoli NA, Italy
XEPTAGEN S. p. A, Via A. Olivetti 1, Pozzuoli NA, Italy
References:
Not available.
Curr Drug Targets (ISSN: 1389-4501), 2002 Jun; 3(3): 223-228.
Export to BibTeX Export to EndNote
Paper type: Journal Article,
Impact factor: 3.597, 5-year impact factor: 3.558
Url: http://www.scopus.com/inward/record.url?eid=2-s2.0-0036001051&partnerID=40&md5=f20fb6aa35c6d58abf643f305ae56dcf
Keywords: Antiidiotypic Antibody, Antiinflammatory Agent, Antimalarial Agent, Azathioprine, Cd16 Antigen, Chymotrypsin, Complement, Corticosteroid, Cyclophosphamide, Cyclosporin, Fc Receptor, Glucocorticoid, Immunoglobulin G, Immunosuppressive Agent, Methotrexate, Monoclonal Antibody, Pepsin A, Tetramer, Tg 19320, Tripeptide Derivative, Unclassified Drug, Oligopeptide, Acquired Immune Deficiency Syndrome, Animal Experiment, Animal Model, Antigen Antibody Complex, Autoimmune Disease, Cataract, Combinatorial Chemistry, Controlled Study, Depression, Disease Predisposition, Drug Bioavailability, Drug Blood Level, Drug Efficacy, Drug Formulation, Drug Half Life, Drug Mechanism, Drug Stability, Drug Synthesis, Drug Targeting, Drug Urine Level, Effector Cell, Female, Glomerulonephritis, Human, In Vivo Study, Infection, Inflammation, Insomnia, Kidney Injury, Microbial Immunity, Molecular Interaction, Mouse, Mouse Strain, Multiple Myeloma, Nausea And Vomiting, Nonhuman, Osteoporosis, Pathogenesis, Review, Rheumatoid Arthritis, Systemic Lupus Erythematosus, Tissue Injury, Validation Process, Weight Gain, Metabolism, Pathophysiology,
Affiliations:
*** IBB - CNR ***
XEPTAGEN S.p.A, Via A. Olivetti 1, Pozzuoli NA, Italy
XEPTAGEN S. p. A, Via A. Olivetti 1, Pozzuoli NA, Italy
References:
Not available.
Novel molecular targets for systemic lupus erythematosus
For a long time the complement cascade has been believed to be the predominant pathway to inflammation and tissue destruction in autoimmune diseases such as systemic lupus erythematosus. Recently, new evidences show that FcRs may share the primacy with complement cascade, playing an equal or greater role in the disease process. The generation of specific mouse strains deficient in individual components has clarified the different role played by complement and Fc receptors in their interaction with ICs, illustrating that complement is essential for innate immunity against microbial pathogens, requiring natural antibodies to mediate its protective effects, whereas FcγRs have evolved as the principal system for coupling antigen-antibody complexes to effector cells and initiate the inflammatory cascade. Validation of FcRs as new therapeutic targets for autoimmune diseases, in particular for Systemic Lupus Erythematosus (SLE), has been provided by a large number of studies where the biological action of soluble forms of FcγRs or of monoclonal antibodies targeting Fc receptors has been assessed. Additional support to the role of FcRs in SLE has been provided by data obtained with compounds derived from combinatorial chemistry, such as TG19320, a tetrameric tripeptide which interferes with IgG/FcγR interaction in vitro and prevents glomerulonephritis in vivo in a SLE susceptible mouse strain. These findings might open the way to new therapeutic approaches for disorders where the role of FcRs has been established, including not only autoimmune diseases like systemic lupus erythematosus, rheumatoid arthritis, multiple myeloma, but also acquired immunodeficiency syndrome (AIDS).
For a long time the complement cascade has been believed to be the predominant pathway to inflammation and tissue destruction in autoimmune diseases such as systemic lupus erythematosus. Recently, new evidences show that FcRs may share the primacy with complement cascade, playing an equal or greater role in the disease process. The generation of specific mouse strains deficient in individual components has clarified the different role played by complement and Fc receptors in their interaction with ICs, illustrating that complement is essential for innate immunity against microbial pathogens, requiring natural antibodies to mediate its protective effects, whereas FcγRs have evolved as the principal system for coupling antigen-antibody complexes to effector cells and initiate the inflammatory cascade. Validation of FcRs as new therapeutic targets for autoimmune diseases, in particular for Systemic Lupus Erythematosus (SLE), has been provided by a large number of studies where the biological action of soluble forms of FcγRs or of monoclonal antibodies targeting Fc receptors has been assessed. Additional support to the role of FcRs in SLE has been provided by data obtained with compounds derived from combinatorial chemistry, such as TG19320, a tetrameric tripeptide which interferes with IgG/FcγR interaction in vitro and prevents glomerulonephritis in vivo in a SLE susceptible mouse strain. These findings might open the way to new therapeutic approaches for disorders where the role of FcRs has been established, including not only autoimmune diseases like systemic lupus erythematosus, rheumatoid arthritis, multiple myeloma, but also acquired immunodeficiency syndrome (AIDS).
Novel molecular targets for systemic lupus erythematosus
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Novel molecular targets for systemic lupus erythematosus
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15 Records (13 excluding Abstracts).
Total impact factor: 62.997 (56.238 excluding Abstracts).
Total 5 year impact factor: 57.132 (50.291 excluding Abstracts).
Total impact factor: 62.997 (56.238 excluding Abstracts).
Total 5 year impact factor: 57.132 (50.291 excluding Abstracts).
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