IgG subclass levels of sera from 26 patients with juvenile chronic arthritis (JCA) were determined by means of mouse monoclonal antibodies. Patients were divided into three groups according to clinical activity of the disease: active disease, partial remission, and remission. One hundred and sixty four age matched, healthy children served as controls. IgG subclass concentrations were log transformed, and a robust regression method was applied to obtain expected values for the different ages. We found a significant increase of IgG3 (p less than 0.0001), IgG1 (p less than 0.002), and IgG2 (p less than 0.035) in JCA sera, while IgG4 values did not differ significantly from those of controls. When patients were divided according to clinical activity significant increases of IgG2 and IgG4 were observed in the patients in partial remission. Our data suggest that differential increase of IgG subclasses during the courses of JCA may be of relevance to the pathogenesis of the disease.
A sensitive enhancing system was developped for detecting low density cell surface antigens by flow cytometry. The system termed “super avidin biotin system” (SABS) uses (i) biotinylated antibody, (ii) phycoerythrin-streptavidin, (iii) biotinylated goat anti streptavidin antibody, and (iiii) phycoerythrin-streptavidin. Antigenic sites of receptors for the C3b complement component (CR1, CD35) were quantified on erythrocytes from healthy individuals and patients infected by human immuno-deficiency virus using SABS and a conventional radio-immunoassay (RIA). As little as 50 sites/ cell were detected using either SABS or RIA. Accurate quantification of antigenic sites were achieved within the range of 100-1300 sites per cell. Intra assay and day to day reproducibilities using SABS were 2 % and 12 % respectively, comparable to those of conventional RIA measurements. In addition to the enumeration of CR1 on erythrocytes for clinical purposes, the use of SABS may be extended to a large number of situations where a sensitive detection of low density cell surface antigen is needed
Earlier investigators have shown that a high serum concentration of IgG2 and a high IgG2 antibody response to several polysaccharide antigens is associated with the allotype G2m(n) of the IgG2 subclass. We now show that the total IgG2 concentrations are significantly higher in G2m(n) than in G2m(–n) homozygotes (difference of means was 1.26‐fold, p = 0.002). Furthermore, in G2m(n) heterozygotes, the G2m(n) allele contributed more than the G2m(–n) allele to specific IgG2 antibody responses and to the total IgG2.
The concentrations of subclasses of IgG in sera from children as reported by several groups were analyzed. A 4th degree polynomial regression curve was calculated for the upper and lower ranges of the subclasses at various ages. In addition percentile values were calculated. The calculated ranges were tested for their usefulness when looking for immunoglobulin subclass deficiencies. In relation to the calculated ranges the sera from 85 controls did not show decreased concentrations of IgG1 or IgG3. Eight % of the sera showed decreased IgG2 and no evaluation was possible for IgG4. We conclude that the calculated ranges of the IgG subclasses are useful for further research on IgG subclass deficiencies
A synthetic peptide of 21 amino acids, homologous to the hinge of the human IgG2 molecule was used for immunization of mice to produce anti-IgG-2 subclass specific monoclonal antibodies. Two monoclonal antibodies of mouse IgG1 and IgM isotype were produced recognizing the IgG2 molecule under various assay conditions. The determinants recognized are located on the Fc and Fab portion of the heavy chain respectively. The IgG2 specific amino acid substitutions are located on the carboxy terminal part of the peptide. Immunization with this determinant, in a short peptide (10 amino acids), on itself did not lead to IgG2 specific antibody responses. A second determinant to the amino terminal side of the peptide to which specific antibodies could be produced appears necessary for the induction of structural elements mimicking the native protein
The excessive intake of alcohol is associated with various changes in both cellular and humoral immunity. Especially notable are the effects of alcohol on the IgA immune system. These include an increase of serum IgA with a slight shift towards IgA2 in the IgA1:IgA2 ratio, the presence of IgA containing immune complexes in the circulation, deposition of IgA in various tissues and an increase in the number of IgA producing cells in the circulation. Some of these features are related to the alcohol etiology while others are related to the severity of liver parenchymal damage, underlining the pivotal role of this organ in the IgA metabolism. Alcohol can disturb the integrity of intestinal mucosa resulting in an increased invasion of antigens from the gut, which will lead to a stimulation of the secretory immune system in particular. The characteristic deposition pattern of IgA along the liver sinusoids, seen in alcoholics, is not a reflection of changes in the circulation but the result of a direct effect of alcohol on the liver. This feature can be used for diagnostic purposes. The pathogenetic relevance of most of these changes in the IgA immune system is still unclear
The ability of long-term survivors of BMT to produce antibodies in vivo to commonly encountered environmental antigens was investigated particularly with respect to the IgG subclass distribution of such responses. The antigens selected were E. coli, pneumococcal polysaccharide and diphtheria toxoid. Sera from 17 normal volunteer donors all showed measurable titres to these antigens and were used as controls. All IgM responses in 17 BMT patients were significantly lower than in controls as were all IgA responses except that to diphtheria toxoid. IgG responses were generally less depressed but when subclasses were examined IgG1 was well maintained but poor responses were seen in all other subclasses
