PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 4435959

Type-specific opsonic antibodies in streptococcal pyoderma.

A L Bisno·K E Nelson
View original source ↗Export metadata ↓

Abstract

Prospective studies of streptococcal pyoderma were carried out among black children enrolled in Project Headstart centers in Holmes County, Miss. Sera collected from 28 of these children in early October were tested for opsonic antibodies to one of two prevalent skin strains of group A streptococci isolated from them on one or more occasions over the preceding 3 months. The two streptococcal strains (A and B) belong to M-types previously unrecognized. Ten subjects (36%) had antibody to their homologous serotypes detectable by the indirect bactericidal test: this included 6 of 10 subjects infected with strain B but only 4 of 18 infected with strain A (P < 0.05). Of 17 children who had strains A or B isolated from skin lesions only, 12% developed type-specific antibodies (TSA) against the infecting serotype. In contrast, 11 subjects had these strains isolated from throat cultures (either with or without associated pyoderma), and 72% had detectable TSA (P < 0.01). There was no demonstrable relationship between the development of antibodies to streptococcal extracellular products or to non-type-specific cellular antigens and the development of TSA. These results demonstrate that type-specific immune responses do occur following infection with pyoderma streptococci. The frequency with which such antibodies develop is variable and appears related to a number of factors, including the immunologic properties of the infecting strain and the site of bacterial colonization. Pharyngeal carriage may represent an important mechanism for development of acquired immunity to skin strains of group A streptococci.

Explore related subjects

Antibody SpecificityBlood Bactericidal ActivityChildChild, PreschoolEpidemiologic MethodsHumansOpsonin ProteinsPharynxPyodermaSerotypingStreptococcal InfectionsStreptococcusJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

A L Bisno, K E Nelson. 1974. Type-specific opsonic antibodies in streptococcal pyoderma.. https://doi.org/10.1128/iai.10.6.1356-1361.1974

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed1997

tea1 and the microtubular cytoskeleton are important for generating global spatial order within the fission yeast cell.

Fission yeast cells identify and maintain growing regions exactly opposed at the ends of a cylindrical cell. tea1 mutants disrupt this organization, producing bent and T-shaped cells. We have cloned tea1 and shown that tea1 is located at the cell poles. Microtubules are continuously required to transfer tea1 to the cell ends, and tea1 is located at the ends of microtubules growing toward the cell poles. We suggest that tea1 acts as an end marker, directing the growth machinery to the cell poles. tea1 is down-regulated in cells treated with pheromone that grow toward a mating partner and no longer maintain their ends exactly opposed. tea1 may also influence microtubular organization, affecting the maintenance of a single central axis.

Antibody Specificity↗
PubMed1997

The inhibitor antibody response is more complex in hemophilia A patients than in most nonhemophiliacs with factor VIII autoantibodies. Recombinate and Kogenate Study Groups.

Approximately 25% of hemophilia A patients infused with factor VIII (fVIII) mount an immune response, which leads to its inactivation. Anti-fVIII autoantibodies are also seen rarely in individuals with normal fVIII. We have previously demonstrated that some anti-A2 and anti-C2 domain antibodies are fVIII inhibitors and that many patients have additional inhibitors with a fVIII light chain (LCh) epitope outside C2. Because the contribution of the different antibodies to the plasma inhibitor titer had been examined in a limited number of patients (14), we report in this study a more extensive analysis of 55 plasmas. The dominant inhibitors in 62% (13 of 21) of autoantibody plasmas were directed only against C2 or A2, but not both, whereas this pattern was found in only 15% (5 of 34) of hemophilic plasmas. In addition, anti-A2 inhibitors were present in 71% (24 of 34) of hemophilic plasmas, but only 33% (7 of 21) of autoantibody plasmas. These results demonstrated that the inhibitor response in hemophiliacs was more complex and the epitope specificity was somewhat different. A comparison of hemophiliacs treated only with plasma fVIII or recombinant fVIII showed no significant differences in the complexity of the inhibitor response, as > or = 2 different inhibitor antibodies were present in 78% (18 of 23) of the former and 82% (9 of 11) of the latter. In contrast, the major inhibitors in 35% (8 of 23) of hemophiliacs treated with plasma fVIII were directed against C2 and another LCh epitope within residues 1649-2137, but not A2, while none (0 of 11) treated with recombinant fVIII had this pattern.

Antibody Specificity↗
PubMed1997

Epitope specificity of HLA class I alloantibodies: II. Stability of cross-reactive group antibody patterns over extended time periods.

The stability of HLA alloantibodies was studied in 128 antibody-positive, potential kidney transplant recipients over an average period of 3 years. Antibody detection was performed using an anti-human globulin-complement-dependent cytotoxicity technique. In this study, the specificity of antibodies was categorized as against either private epitopes or cross-reactive group (CREG) epitope clusters. Definable antibodies were found in 94% of patients, and 89.5% of the definable antibodies had specificity for CREG clusters. Patterns of antibody reactivity were stable in most of the patients evaluated, even though the percentage of panel-reactive antibody (PRA) often demonstrated considerable fluctuations. Of the 220 definable private-specific or CREG cluster-specific antibodies identified in the patients, nearly 80% persisted throughout the observation period. The fluctuations in % PRA were common, but usually were not due to the acquisition of new HLA antibodies. Most fluctuations were attributable to variable detection of specificities within the same CREG cluster, possibly due to technique variation or changes in antibody avidity or titer or in cell panel composition. This study demonstrates that patterns of antibody specificity are remarkably stable in this patient population, even though PRA values fluctuated. This study further suggests that HLA antibody specificity analysis is a more useful clinical parameter of lymphocytotoxicity testing than simple reporting of % PRA when identifying potential donors for individual patients.

Antibody Specificity↗