acid-phosphatase and Autoimmune-Diseases

Topics: Acid Phosphatase; Animals; Autoimmune Diseases; Bacterial Infections; Ejaculation; Epididymis; Genital Diseases, Male; Genitalia, Male; Humans; Infertility, Male; Male; Methods; Prostate; Radiography; Semen; Seminal Vesicles; Species Specificity; Urinary Bladder; Vas Deferens

Topics: Acid Phosphatase; Adult; Animals; Antibody Specificity; Antigen-Antibody Complex; Arthus Reaction; Autoantibodies; Autoimmune Diseases; Basement Membrane; Binding Sites; Chemotaxis; Complement System Proteins; Elastic Tissue; Electrophoresis, Disc; Epithelium; Female; Fluorescent Antibody Technique; Glomerulonephritis; Haplorhini; Humans; Immune System Diseases; Immunization, Passive; Immunoglobulin G; Leukocytes; Lysosomes; Male; Microbial Collagenase; Pancreatic Elastase; Protein Binding; Serum Sickness; Skin Diseases

Topics: Acid Phosphatase; Adenosine Triphosphatases; Alkaline Phosphatase; Autoimmune Diseases; Autoradiography; Biopsy; Chronic Disease; Gastric Juice; Gastric Mucosa; Gastritis; Glycosaminoglycans; Histocytochemistry; Humans; Microscopy, Electron; Mitosis; NAD; NADP; Oxidoreductases; Pyrophosphatases; RNA

Spondyloenchondrodysplasia (SPENCD) is a rare skeletal dysplasia, characterized by metaphyseal lesions, neurological impairment and immune dysregulation associated with lupus-like features. SPENCD is caused by biallelic mutations in the ACP5 gene encoding tartrate-resistant phosphatase. We report on a child, who presented with spasticity, multisystem inflammation, autoimmunity and immunodeficiency with minimal metaphyseal changes due to compound heterozygosity for two novel ACP5 mutations. These findings extend the phenotypic spectrum of SPENCD and indicate that ACP5 mutations can cause severe immune dysregulation and neurological impairment even in the absence of metaphyseal dysplasia.

Topics: Acid Phosphatase; Autoimmune Diseases; Autoimmunity; Bone Diseases; Child; Female; Humans; Immunologic Deficiency Syndromes; Inflammation; Isoenzymes; Magnetic Resonance Imaging; Muscle Spasticity; Mutation; Osteochondrodysplasias; Tartrate-Resistant Acid Phosphatase; Tomography, X-Ray Computed

Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by bone erosion and cartilage destruction in the joints. Many of the conventional antiarthritic drugs are effective in suppressing inflammation, but they do not offer protection against bone damage. Furthermore, the prolonged use of these drugs is associated with severe adverse reactions. Thus, new therapeutic agents that can control both inflammation and bone damage but with minimal side effects are sought. Celastrus is a Chinese herb that has been used for centuries in folk medicine for the treatment of various inflammatory diseases. However, its utility for protection against inflammation-induced bone damage in arthritis and the mechanisms involved therein have not been examined. We tested celastrus and its bioactive component celastrol for this attribute in the adjuvant-induced arthritis model of RA. The treatment of arthritic rats with celastrus/celastrol suppressed inflammatory arthritis and reduced bone and cartilage damage in the joints as demonstrated by histology and bone histomorphometry. The protective effects against bone damage are mediated primarily via the inhibition of defined mediators of osteoclastic bone remodeling (e.g. receptor activator of nuclear factor-κB ligand (RANKL)), the deviation of RANKL/osteoprotegerin ratio in favor of antiosteoclastic activity, and the reduction in osteoclast numbers. Furthermore, both the upstream inducers (proinflammatory cytokines) and the downstream effectors (MMP-9) of the osteoclastogenic mediators were altered. Thus, celastrus and celastrol controlled inflammation-induced bone damage by modulating the osteoimmune cross-talk. These natural products deserve further consideration and evaluation as adjuncts to conventional therapy for RA.

Topics: 3T3 Cells; Acid Phosphatase; Animals; Arthritis; Autoimmune Diseases; Bone and Bones; Celastrus; Cell Line; Fibroblasts; Immune System; Inflammation; Isoenzymes; Macrophages; Mice; Pentacyclic Triterpenes; Plant Extracts; Rats; Rats, Inbred Lew; Synovial Membrane; Tartrate-Resistant Acid Phosphatase; Triterpenes

Vertebral and metaphyseal dysplasia, spasticity with cerebral calcifications, and strong predisposition to autoimmune diseases are the hallmarks of the genetic disorder spondyloenchondrodysplasia. We mapped a locus in five consanguineous families to chromosome 19p13 and identified mutations in ACP5, which encodes tartrate-resistant phosphatase (TRAP), in 14 affected individuals and showed that these mutations abolish enzyme function in the serum and cells of affected individuals. Phosphorylated osteopontin, a protein involved in bone reabsorption and in immune regulation, accumulates in serum, urine and cells cultured from TRAP-deficient individuals. Case-derived dendritic cells exhibit an altered cytokine profile and are more potent than matched control cells in stimulating allogeneic T cell proliferation in mixed lymphocyte reactions. These findings shed new light on the role of osteopontin and its regulation by TRAP in the pathogenesis of common autoimmune disorders.

Topics: Acid Phosphatase; Autoimmune Diseases; Autoimmunity; Bone and Bones; Bone Diseases, Developmental; Brain; Calcium; Child; Genetic Predisposition to Disease; Homozygote; Humans; Isoenzymes; Male; Mutation; Osteochondrodysplasias; Osteopontin; Phosphorylation; Radiography; Tartrate-Resistant Acid Phosphatase

Topics: Acid Phosphatase; Alleles; Autoantibodies; Autoimmune Diseases; Autoimmunity; Brain; Genes, Recessive; HLA Antigens; Humans; Isoenzymes; Lupus Erythematosus, Systemic; Mutation; Osteochondrodysplasias; Osteopontin; Phosphorylation; Risk; Syndrome; Tartrate-Resistant Acid Phosphatase

Prostatic acid phosphatase (PAP) is uniquely expressed in prostatic tissue and prostate cancer. In this study, the immunogenicity of PAP was investigated in a male rat model. We show that immunization with recombinant rat or human PAP in CFA leads to a significant Ab response, but does not generate CTL or result in autoimmune prostatitis. In contrast, immunization with recombinant vaccinia expressing human PAP, but not rat PAP, generates a CTL response and tissue-specific prostatitis in the absence of detectable PAP-specific Abs. These findings suggest that a cellular immune response to PAP, rather than Abs, mediates destructive autoimmune prostatitis. Thus, xenogeneic forms of PAP are a new tool for the induction of prostate-specific immunity and may prove useful for the immunotherapy of prostate cancer.

Topics: Acid Phosphatase; Animals; Autoimmune Diseases; Humans; Immunotherapy, Active; Injections, Intravenous; Injections, Subcutaneous; Male; Organ Specificity; Prostate; Prostatic Neoplasms; Prostatitis; Rats; Rats, Inbred Strains; Tumor Cells, Cultured; Vaccines, Synthetic; Vaccinia virus

Our previous study reported the rich existence of multinucleated giant cells in an autoimmune myocarditis experimentally induced in rats. The present study investigated the histochemical and ultrastructural characteristics of these giant cells. Histochemistry for an acid phosphatase clearly demonstrated multinucleated giant cells dispersed at the inflammatory foci. Ultrastructurally, the giant cells were shown to be single cells, but not clustered cells. Their ultrastructural characteristics were very similar to the basic features of macrophages, except that the giant cells were poor in lysosomes and phagosomes. It was noticeable that some macrophages possessed three or more nuclei, displaying an intermediate form between mononuclear macrophages and multinucleated giant cells. These findings suggest that the giant cell in the experimental autoimmune myocarditis is a single multinucleated cell, and possibly derived from macrophages by cell-to-cell fusion.

Topics: Acid Phosphatase; Animals; Autoimmune Diseases; Cell Fusion; Disease Models, Animal; Giant Cells; Macrophages; Male; Myocarditis; Rats; Rats, Inbred Lew

Macrophages isolated from fish undergoing an experimentally induced autoimmune response against the testis were found to have been activated using several morphological and functional criteria. They exhibited increases in cell spreading, phagocytosis, reduction of nitroblue tetrazolium and acid phosphatase activity. In addition they possessed larger and more numerous cytoplasmic organelles and peripheral processes compared with control cells. Culture of the autoimmunologically elicited cells for 1 or 2 days resulted in their return to a non-activated state.

Topics: Acid Phosphatase; Animals; Autoimmune Diseases; Macrophage Activation; Macrophages; Male; Nitroblue Tetrazolium; Orchitis; Phagocytosis; Salmonidae; Time Factors; Trout

Topics: Acid Phosphatase; Animals; Autoimmune Diseases; Guinea Pigs; Retinitis; Uveitis

Topics: Acid Phosphatase; Adolescent; Adult; Aged; Arthritis, Rheumatoid; Autoimmune Diseases; Female; Humans; Lymphocyte Activation; Male; Middle Aged; Osteoarthritis; Rheumatic Diseases

Topics: Acid Phosphatase; Autoimmune Diseases; Epididymis; Fructose; Genital Diseases, Male; Humans; Male; Orchitis; Sperm Agglutination; Spermatozoa

Topics: Acid Phosphatase; Animals; Atrophy; Autoimmune Diseases; Endoplasmic Reticulum; Esterases; Histocytochemistry; Hyperplasia; Infertility, Male; Lymphocytes; Macrophages; Male; Microscopy, Electron; Organ Size; Phagocytosis; Rats; Spermatozoa; Testis

Topics: Acid Phosphatase; Aminopeptidases; Animals; Antigens; Autoimmune Diseases; Cathepsins; Deoxyribonucleases; Disease Models, Animal; Glucuronidase; Guinea Pigs; Hyaluronoglucosaminidase; L-Lactate Dehydrogenase; Leucine; Lysosomes; Male; Organ Size; Oxidoreductases; Ribonucleases; Sorbitol; Spermatogenesis; Spermatozoa; Testis

Topics: Acid Phosphatase; Animals; Antibodies; Antigen-Antibody Reactions; Autoimmune Diseases; Complement System Proteins; Ferritins; gamma-Globulins; In Vitro Techniques; Liver; Lysosomes; Microscopy, Electron; Mitochondria; Oxidative Phosphorylation; Rabbits; Rats