ABSTRACT
Experimental data have established that HIV-infected lymphocytes activate the complement system. However, because mammalian lymphocytes possess a series of cell-surface complement regulators that inhibit amplification on autologous cells, complement-mediated destruction of host cells is usually inhibited. These studies were performed to examine whether alterations in the cell-surface complement regulatory proteins decay-accelerating factor (DAF, CD55) and membrane cofactor protein (MCP, CD46) may occur during HIV infection in vitro or in vivo. The physiologic significance of these alterations were assessed by radiolabeled chromium release experiments. We show that MCP fluorescent intensity is significantly lessened in HIV-infected children and that DAF intensity is similarly lessened in infected children with advanced disease. These findings could be duplicated with HIV infection of peripheral blood mononuclear cells in vitro.
Subject(s)
Antigens, CD/biosynthesis , Complement Inactivator Proteins/biosynthesis , HIV Infections/immunology , HIV-1 , Leukocytes, Mononuclear/immunology , Membrane Glycoproteins/biosynthesis , Adult , CD55 Antigens , Cell Line , Cells, Cultured , Child, Preschool , Complement System Proteins/biosynthesis , Enzyme-Linked Immunosorbent Assay , Female , Fluorescent Antibody Technique , Humans , Infant , Leukocytes, Mononuclear/virology , Male , Membrane Cofactor Protein , Receptors, Virus/biosynthesisABSTRACT
We investigated the potential role of the complement system in juvenile rheumatoid arthritis (JRA) by examining plasma for levels of complement activation fragments C4d and Bb. We correlated findings with both disease activity and laboratory abnormalities, including immune complex (IC) levels. While there was a strong correlation between active disease and both C4d and Bb plasma levels in JRA, no strong correlations could be made between IC levels and complement activation products; weak associations were seen between complement activation fragments and erythrocyte sedimentation rate. Our data suggest that plasma complement activation is a concomitant of active disease in JRA; however, its role in the pathophysiology of JRA remains uncertain.
Subject(s)
Antigen-Antibody Complex/analysis , Arthritis, Juvenile/immunology , Complement Activation , Complement C4b , Arthritis, Juvenile/blood , Autoantibodies/analysis , Blood Sedimentation , Child , Complement C4/analysis , Complement Factor B/analysis , Enzyme-Linked Immunosorbent Assay , Female , Humans , Male , Peptide Fragments/analysisABSTRACT
This study was undertaken to determine the clinical relevance of IgM rheumatoid factors (RFs) detected by enzyme-linked immunosorbent assay (ELISA) in children with juvenile rheumatoid arthritis (JRA) by examining their association with severity of acute articular disease. ELISAs for IgM-RF were performed on serum specimens from 65 children with JRA. Activity of articular disease was estimated by an arbitrary scoring system. Significant differences were seen in articular disease activity between the group of children with polyarticular disease who were IgM-RF-positive by ELISA compared with those who were IgM-RF-negative (P = .0003). When a small group of individual children with polyarticular disease were followed longitudinally, similar correlations were found between severity of acute disease and the presence of IgM-RFs detected by ELISA. In children with pauciarticular JRA, expression of IgM-RFs appeared to be a transient phenomenon with no correlation with either articular disease or laboratory abnormalities.
