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At least 19 recordsLinked to original sources
PubMed1989

Maturation of immunoglobulin G avidity after rubella vaccination studied by an enzyme linked immunosorbent assay (avidity-ELISA) and by haemolysis typing.

Two tests were introduced recently for assessment of the avidity of rubella immunoglobulin antibodies. In the quantitative test--avidity-enzyme linked immunosorbent assay (ELISA)--IgG antibodies obtained from individuals shortly after primary infection with rubella virus are distinguished from those with past immunity by their antigen-elution characteristics. This method uses agents that disrupt hydrophobic bonds in proteins [Kamoun PP (1988): Denaturation of globular proteins by urea: Breakdown of hydrophobic bonds? Trends in Biological Sciences 13:424-425.]. In the semiquantitative, presumptive test--haemolysis typing--the low-avidity rubella-IgG antibodies are distinguished from the high-avidity antibodies by the quality of their haemolytic zones in a radial haemolysis test. In the present study, both tests were applied to sera taken before and after vaccination with two different strains (Cendehill or RA 27/3) of live attenuated rubella virus. It was found that after vaccination of previously nonimmune subjects, IgG synthesized during the first 2 months had a very low avidity; IgG avidity increased dramatically during the subsequent 4 months and less markedly between 6 and 12 months after vaccination. On the contrary, the initially high IgG avidity of previous immune vaccinees remained at an elevated level postvaccination. These results provide a basis for identification of recent primary rubella virus infections, or vaccination reactions, by the avidity of specific IgG and also for their separation from rubella reinfections.

Adult↗
PubMedDate not supplied

Rubella IgG total antibody avidity and IgG subclass-specific antibody avidity assay and their role in the differentiation between primary rubella and rubella reinfection.

The total rubella IgG antibody avidity ELISA, as described by Hedmann for differentiation between acute primary rubella and reinfection, persisting or non-specific IgM antibodies were evaluated in 212 sera of four categories of patients with known history (n = 149) and in one group (n = 39) of patients with a history of unclear nature. The development of the IgG ratio (avidity) from low (less than 30%) to higher levels (greater than 30%) was determined in 146 sera from 96 cases with acute primary rubella between days 1 to 256 after onset of exanthem, with a borderline between low (less than 30%) and high (greater than 30%) avidity after four weeks after onset of exanthem. From seven days to 14 years following vaccination, the IgG ratio increased more slowly following vaccination, with a useful borderline at 2 1/2 months. In 80 sera from 13 women with reinfection during pregnancy, six infants with rubella embryopathy, and 19 pregnant women with rubella IgM antibodies detected during antenatal screening, the total IgG ratio ranged between 48% and 100%, indicating a previous infection. The diagnostic value of the IgG subclass-specific antibody avidity assay was investigated in 40 of the 251 sera. The results confirmed those of the total IgG avidity assay. Both tests are of additional help for differentiating serologically primary rubella from reinfection or recent from previous vaccination.

Adolescent↗
PubMed1977

Avidity of anti-DNA antibodies in serum and IgG glomerular eluates from patients with systemic lupus erythematosus. Association of high avidity antinative DNA antibody with glomerulonephritis.

Significant differences in both specificity and avidity of anti-DNA antibodies were observed in the sera of groups of patients with active systemic lupus erythematosus glomerulonephritis, active systemic lupus erythematosus without nephritis, and in IgG eluates obtained by DNAase digestion of isolated glomeruli from glomerulonephritic kidneys. With methylated albumin-kieselguhr fractionated 3H-HeLa DNA as a source of native or single-strand DNA antigen in a modified Farr assay, an increased level of antibody to native DNA was associated with active systemic lupus erythematosus, particularly active nephritis. The avidity of antinative DNA estimated from plots of the reciprocals of bound and free antigen according to the Sips distribution formula was significanly lower in active glomerulonephritis sera than in sera from patients with active systemic lupus erythematosus without nephritis. However, antinative DNA of uniformly high avidity was found in the glomerular eluates. Avidity of single-strand DNA antibodies did not differ in the various patient groups. The data stronly supprot a major role for high avidity antinative-DNA in DNA/antiDNA immune complex-induced glomerular injury in systemic lupus erythematosus.

Antibodies, Anti-Idiotypic↗
PubMed1992

Regulation of LFA-1 avidity in human B cells. Requirements for dephosphorylation events for high avidity ICAM-1 binding.

Regulation of the avidity of LFA-1 (CD11a/CD18, alpha L beta 2) for its ligand ICAM-1 (CD54) was studied in human B cells by evaluating the effects of a phorbol ester, anti-IgM antibodies, staurosporine, and okadaic acid. We monitored changes in LFA-1 avidity by quantifying binding of cells to an immobilized rICAM-1 fusion protein. In this assay, the protein kinase C-activating phorbol ester PDB and anti-IgM antibodies, as well as the protein kinase inhibitor, staurosporine, were able to induce LFA-1-dependent binding to ICAM-1. This demonstrates that the high avidity state of LFA-1 can be induced by a protein kinase C-dependent and by a protein kinase C-independent pathway. Furthermore, treatment of the cells with the protein phosphatase inhibitor, okadaic acid, inhibited binding to ICAM-1. Treatment with staurosporine before addition of okadaic acid not only induced enhanced binding of cells to ICAM-1, but also dramatically reduced the ability of okadaic acid to inhibit binding. These results suggest a critical role for a protein phosphatase in inducing the high avidity state of LFA-1 as well as a role for a protein kinase in inducing the low avidity state of LFA-1.

Alkaloids↗
PubMed1992

Avidity and bactericidal activity of antibody elicited by different Haemophilus influenzae type b conjugate vaccines. The Vaccine Study Group.

OBJECTIVE: Antibody avidity is a measure of the functional affinity of serum antibody to bind to antigen. In this study, we compared the avidity of antibodies elicited by vaccination with three Haemophilus influenzae type b (Hib) conjugate vaccines and investigated the relationship between antibody avidity and the ability of antibody to activate complement-mediated bactericidal activity. DESIGN: A convenience sample of 171 postvaccination serum samples with more than 0.5 microgram/mL of anticapsular antibody, the minimum concentration required for measurement of avidity. The serum samples were obtained from infants participating in immunogenicity trials with Hib capsular polysaccharide (PRP) conjugated to meningococcal outer membrane protein complex (PRP-OMPC) or to tetanus toxoid (PRP-T), or PRP oligomers conjugated to a nontoxic mutant diphtheria toxin, CRM197 (Oligo-CRM). PATIENTS: Healthy infants recruited in private practices. PRIMARY OUTCOME MEASURES: Avidity of vaccine-induced serum anticapsular antibody and serum bactericidal titers. RESULTS: In infants vaccinated at 2, 4, and 6 months of age, Oligo-CRM evoked antibody of higher avidity than PRP-OMPC (P less than .001). The mean avidity of antibody elicited by PRP-T was intermediate, being lower than Oligo-CRM (P less than .02) but higher than PRP-OMPC (P = .001). Also, after one dose, 18-month-old infants given Oligo-CRM had higher avidity antibodies compared with those given PRP-OMPC (P less than .001). Half of the infants in both age groups who were given Oligo-CRM developed antibody avidity of 2.50 nM-1 or greater, whereas more than two thirds of the infants given PRP-OMPC had avidity values of 1.25 nM-1 or less. Antibodies with avidity of 1.25 nM-1 or less were, on average, 6.6-fold less active in assays of complement-mediated bactericidal activity than antibodies with avidity of 2.50 nM-1 or greater (P less than .001). CONCLUSIONS: Oligo-CRM and PRP-T conjugate vaccines elicit higher avidity antibody than PRP-OMPC, and high-avidity antibody is more potent than low-avidity antibody in serum bactericidal assays. Consideration should be given to including measurement of antibody avidity in assessment of new vaccines since avidity may affect the ability of serum antibody to confer protection against disease.

Antibodies, Bacterial↗
PubMed1989

Measurement of avidity of specific IgG for verification of recent primary rubella.

Sixty-four subjects' serum samples, positive or equivocal by rubella IgM assays and containing rubella IgG, were examined for the avidity of rubella IgG. Four of the sera originated from rubella reinfections; others had false-positive IgM results due to interference by parvovirus infection or by other mechanisms; and the remaining were sera from the acute phase or convalescence of primary rubella. A novel IgG avidity test, avidity-ELISA, and a semiquantitative haemolysis typing assay were used. According to the avidity-ELISA, 29 subjects had recent primary rubella (low IgG avidity), and another 29 had previous rubella immunity (high IgG avidity), whereas 6 serum samples gave borderline avidity values. Comparison of these results with pre-existing clinical records and laboratory data showed that all samples with low IgG avidity were obtained during or shortly after acute primary rubella. All sera with high IgG avidity originated from the previously immune subjects; the rubella reinfections were confined within this group. Five of the six sera with borderline avidity values were obtained within 2 months from primary rubella. In conclusion, the measurement of IgG avidity is a powerful tool for the distinction of acute or recent primary rubella from pre-existing rubella immunity, including rubella reinfections.

Adult↗
PubMed1974

Isolation of antigen-binding cells from unprimed mice: demonstration of antibody-forming cell precursor activity and correlation between precursor and secreted antibody avidities.

Cells binding DNP groups conjugated to fluoresceinated mouse gamma globulin ((F)DNP-MGG) were isolated from spleens of unprimed mice using a fluorescence-activated cell sorter (FACS). The isolated cells were specifically enriched at least 100-fold for anti-DNP precursor activity in an adoptive transfer assay as compared to unfractionated spleen. The fraction depleted of binding cells, although depleted of anti-DNP precursor activity, responded as well as unfractionated spleen when assayed for anticarrier (keyhole limpet hemocyanin [KLH]) precursor activity. High avidity binding cells were stained using low concentrations of (F)DNP-MGG. Medium and low avidity binding cells were stained using high concentrations of (F)DNP-MGG in the presence of free hapten which selectively blocked staining of the high avidity binding cells. Cells were supplemented with an excess of carrier-primed (KLH), nylon-purified splenic T cells and transferred to irradiated recipients. DNP-KLH was given at transfer and 5 days later. The anti-DNP plaque-forming cell (DNP-PFC) response and the avidities of the DNP-PFC in the irradiated recipients were measured by hapten inhibition of direct PFC plaque formation 12 days after transfer. At this time, very few indirect PFC were found. There was a positive correlation between the avidity of the DNP-binding cells and the avidity of the anti-DNP antibody secreted by their progeny. High avidity DNP-binding cells gave rise to predominantly high avidity anti-DNP-PFC. Medium and low avidity binding cells gave rise to medium and low avidity DNP-PFC.

Animals↗
PubMed1975

Antibody avidity for native DNA in lupus nephritis.

To study the participation of the antibody avidity in the pathogenesis of lupus nephritis, we measured the antibody avidity to native DNA by the method of Minden and Farr (14) in patients with SLE. The avidity to native DNA was almost less than 40%. The avidity and the histological activity of lupus nephritis were well correlated; the antibody avidity of the active-group sera was higher than that of the inactive-group sera and the group without nephritis. In the group with antibodies of relatively high avidity, the complexes were deposited mainly in the subendothelial side of GBM and in the mesangium. On the other hand, in the group with low-avidity antibodies, the complexes were localized in the subepithelial side of GBM. On investigating the quality of the complexes, we noted that the complexes composed of high-avidity antibodies prepared in vitro were larger than those of low avidity and the former were larger than 19S. If the native-DNA-anti-native DNA system is the mechanism basic to lupus nephritis, the differences in immune response of the host, namely the degree of antibody avidity may greatly affect complex formation and influence the histological activity and nephritogenicity of lupus nephritis.

Adult↗
PubMed1992

Antibody avidity in swine lymphocyte antigen-defined miniature pigs.

Antibody avidity to hen egg white lysozyme (HEWL) was measured by thiocyanate ion elution enzyme-linked immunosorbent assay (ELISA) in swine lymphocyte antigen (SLA) defined miniature pigs. Serum antibody avidity was evaluated on day 14 and 30 after primary (day 0) and secondary (day 14) immunizations in eight to ten week old miniature pigs previously typed for swine lymphocyte antigen genotype. The effect of SLA genotype, litter, and gender on anti-HEWL antibody avidity was determined by least squares. Antibody avidity varied amongst individuals. Antibody avidity maturation was observed as a mean rise in antibody avidity from primary response (0.89 +/- 0.64) to secondary response (1.23 +/- 0.54) (p < 0.0005). Overall, SLA genotype did not significantly influence antibody avidity or avidity maturation, but pigs of dd genotype had greater avidity maturation between primary and secondary responses than other genotypes. Litter effects significantly affected antibody avidity and maturation.

Analysis of Variance↗
PubMed1989

Comparison of concentration and avidity of specific antibodies to E. coli in breast milk and serum.

To investigate the relationship between mucosal and systemic immunity we analysed the specific anti-Escherichia coli antibody concentration and avidity of IgA in colostrum and IgG in paired blood samples from 47 mothers giving birth to premature neonates. The avidity of each sample, expressed as an avidity index, was determined using a novel enzyme immunoassay (EIA)-based procedure, while specific antibody determinations were performed by means of conventional sandwich EIA techniques. All subjects had detectable antibody to E. coli in serum and breast milk. The median avidity index for specific IgA antibody in breast milk (3.53 M NH4SCN, range 2.77-4.90) was significantly higher (P less than 0.0001) than that for specific IgG antibody in serum (median 2.03 M NH4SCN, range 1.15-3.65). Using Spearman correlation analysis, a weak but significant association was found between the avidity of colostral IgA antibody and the avidity of systemic IgG antibody to pooled E. coli polysaccharides (rs = 0.29, P = 0.02). There was also a weak correlation between the concentrations of specific serum IgG antibody and of specific colostral IgA antibody (rs = 0.36, P = 0.006). There was no correlation between the concentration of IgA anti-E. coli antibody in colostrum and the avidity of colostral IgA antibody (rs = 0.14, P less than 0.05). Similarly, there was no correlation between the concentration and the avidity of serum IgG anti-E. coli antibody (rs = 0.23, P less than 0.05). The findings of this study suggest independent regulation of concentration and avidity of specific IgA antibody in preterm breast milk. Similar results were seen for specific IgG antibody in serum. The correlations between systemic and mucosal antibody with respect to both concentration and avidity were significant, but are relatively weak and therefore suggest that there also may be independent factors which afford differential regulation of systemic and mucosal antibody responses.

Antibodies, Bacterial↗
PubMed1992

Antibody avidity in Yorkshire pigs of high and low immune response groups.

Avidity indices of antibody to hen egg-white lysozyme (HEWL) were measured by chaotropic ion (SCN-) elution enzyme-linked immunosorbent assay (ELISA) in pigs grouped as high, control or low for various immune and innate resistance-related traits. The avidity index was the molar concentration of SCN- required to reduce by 50% the ELISA optical density value for a given serum. The index was independent of the amount of antibody. Eight- to ten-week-old Yorkshire pigs were immunized with HEWL and serum antibody measured by ELISA as one of five traits used to assign them to high, low or control response groups. Serum antibody avidity for HEWL was evaluated on Day 14 and Day 30 after primary (Day 0) and secondary (Day 14) immunization. The effects of response group, gender, litter, serum IgG concentration and anti-HEWL antibody on avidity were determined using a linear model. Antibody avidity indices varied amongst individuals. Mean avidity indices for sera collected on Days 14 and 30 were 0.61 +/- 0.43 and 1.22 +/- 0.56, with maximum indices of 2.64 and 2.86 respectively. Avidity of secondary response antibody was significantly higher (P less than or equal to 0.05). Pigs of the high response group had significantly higher secondary antibody avidity than those of the control (P less than or equal to 0.08) and low groups (P less than or equal to 0.01). Avidity index was positively correlated with antibody to HEWL on Days 14 and 30 but not to preimmunization serum IgG concentration or to other measured traits.

Animals↗
PubMed1978

Age-dependent variations of antibody avidity.

Age-dependent variations of antibody avidity were studied in the C3HeB/FeJ mouse. Spleen cells from donors of different ages (10--720 days) were transferred and stimulated with TNP-HRBC in lethally irradiated syngenic recipients. The anti-TNP antibody response of the donor cells was estimated from the number of direct PFC per recipient spleen by the Jerne technique with TNP-SRBC. Avidity of the antibodies secreted by PFC was evaluated from the amount of added TNP-BSA that inhibited 50% of the anti-TNP PFC. Under these experimental conditions allowing the exclusion of any influence of the donor milieu during the immune response, age-dependent variations of the antibody response and avidity could be attributed to changes in the donor spleen cell population. Avidity was found to increase with the response and to vary parabolically with age. After appropriate correction of the number of PFC to make it independent from age, avidity values were fitted by a multiple curvilinear regression in which the independent variables playing a significant role were the corrected number of PFC in its linear term and the age in its linear and quadratic terms. From comparison of the standard coefficients of this regression, the observed variations of avidity could be attributed in part (82%) to the response and in part (18%) to the age. For any value of response, avidity increased 15-fold from day 10 to reach a maximum at day 110 and then declined 5-fold at the age of 720 days. Heterogeneity of avidity also changed parabolically with age as high avidity classes were present in adulthood and absent at 10 and 720 days.

Aging↗
PubMed1988

Avidity of IgA antibody to Escherichia coli polysaccharide and diphtheria toxin in breast milk from Swedish and Pakistani mothers.

The avidity of breast milk IgA antibody was studied with the aid of thiocyanate elution of antibody from solid-phase bound E.coli polysaccharides and diphtheria toxoid. The relative avidity index for each sample was determined by the molarity of thiocyanate required to elute 50% of the bound IgA antibody under conditions of antigen excess. Milk samples collected from Pakistani mothers during early lactation (2-4 weeks after delivery; n = 12) had a significantly lower median relative avidity index of IgA antibody to E.coli antigens than did early lactation samples from Swedish mothers (n = 11; avidity indices 1.78 M and 2.65 M; P less than 0.02). Samples collected from Pakistani mothers in mid-lactation showed a significant rise in the relative avidity index to a median of 2.50 M (P less than 0.01), with a subsequent fall in late lactation (28-36 weeks after delivery) to 1.75 M (P less than 0.01). Milk samples from Pakistani mothers in mid-lactation (n = 12) also had a lower median relative avidity index of IgA antibody to diphtheria toxoid than did samples from Swedish mothers (n = 14; avidity indices 2.35 M and 4.30 M; P less than 0.002). The lower avidity of breast milk IgA in Pakistani mothers in comparison with Swedish mothers may arise from differences in antigen exposure or nutritional status or could possibly be genetically determined.

Antibody Affinity↗
PubMed1992

Immunoglobulin G antibody avidity in patients with respiratory syncytial virus infection.

The titer and avidity of respiratory syncytial virus-specific antibodies were measured in 196 serum specimens from 93 children with an acute, laboratory-confirmed respiratory syncytial virus infection. An enzyme immunoassay method based on the ability of urea to dissociate the bound antibodies with low avidity from the antigen was used. Three patterns of immune responses were observed. Children less than 6 months of age usually had low titers of antibodies with high avidity in their acute-phase serum samples. These antibodies were concluded to be of maternal origin, since their reaction pattern was similar to that of healthy adults. During the next few weeks, a slight increase in titers with a concurrent decrease in antibody avidity was observed. All children 6 to 24 months of age had low-avidity antibodies in their acute-phase serum samples, which matured to high avidity during the follow-up. On the contrary, about half of the children greater than 24 months of age had high-avidity antibodies already in the acute-phase serum samples. We conclude that the former children were experiencing primary infections with respiratory syncytial virus and the latter were experiencing reinfections. All adults with remote immunity had antibodies with high avidity.

Adult↗
PubMed1991

The influence of avidity on signaling murine B lymphocytes with monoclonal anti-IgM antibodies. Effects of B cell proliferation versus growth inhibition (tolerance) of an immature B cell lymphoma.

We have investigated the effect of the avidity of a monoclonal anti-mouse IgM antibody (mAb) on its ability to activate normal B cells vs its capacity to inhibit the growth of an immature B lymphoma, BKS-2. A panel of seven mAb with specificities for four different domains of mu-heavy chain were selected and their relative avidities measured. Of the seven mAb studied, four antibodies (b7-6, Ak11, AK15, and DS1) were found to have relatively higher avidities than three others (AK17, 331.12, and Bet-2). Among them, the mAb b7-6 was highly efficient in inducing proliferation of normal B cells, whereas all others (including the remaining three high avidity mAb) were inefficient in inducing B cell proliferation. This failure cannot be simply related to the differences in their fine specificity because all the mAb became highly stimulatory after coupling to Sepharose beads. With one exception (DS1), avidity was a better predictor of the growth-stimulatory capacity when the antibodies were immobilized. Taken together, these findings suggested that although high affinity was important, there were other factors that might influence the mitogenic potential of a soluble anti-mu mAb. On the other hand, all anti-mu mAb irrespective of their avidity, fine specificity, and isotype were capable of effectively inhibiting the growth of BKS-2 cells. Furthermore, there was a direct correlation between the avidity and the dose of the mAb required to cause half-maximal inhibition of BKS-2 growth. The F(ab) fragments of high avidity mAb b7-6 failed to inhibit the growth of BKS-2 cells, which indicates that a minimal level of cross-linking of the membrane Ig receptor is necessary for causing growth inhibition in BKS-2 cells. Although there was no significant difference in the tolerogenic potential of soluble vs immobilized anti-mu mAb in directly inactivating BKS-2 cells, their growth-inhibitory capacity was remarkably different in the presence of rIL-5. Thus, rIL-5 was effective in partially overcoming the tolerogenic effect of soluble but not immobilized anti-mu mAb. Unlike IL-5, LPS rescued BKS-2 cells from the inhibitory effect of both soluble and immobilized anti-mu antibodies. Altogether, these results suggested that the ligand binding requisites for tolerance induction were less stringent than those for B cell activation. Furthermore, a high affinity interaction between membrane Ig receptor and its ligand appeared to generate a dominant negative signal that was not reversed by lymphokines.

Animals↗
PubMed1976

Role of t lymphocytes in the humoral immune response. II. T cell-mediated regulation of antibody avidity.

The effect of activated T lymphocytes (ATC) on the avidity distribution of PFC in the secondary response was studied in normal mice. The total PFC response was not significantly changed for either direct or indirect PFC by administration of ATC before secondary antigen challenge. However, marked suppression occurred of indirect PFC that secreted high avidity antibody; no suppression was seen of high avidity direct PFC. At the same time, significant stimulation was seen of relative and absolute frequencies of indirect PFC that secreted middle and low avidity antibody. These effects were dependent on Thy 1-bearing, nylon nonadherent cells which demonstrated carrier specificity. In further characterization of these effects, it was found that increasing the number of ATC transferred produced progressive loss of high avidity PFC and compensatory increase in lower avidity PFC. Moreover, in these experiments, suppression of the high avidity response was inducible with the administration of ATC 5 weeks before to 3 days after the secondary immunization. Thus, it is likely that the avidity-modifying effects are dependent on T lymphocytes which influence the late stages of B lymphocyte maturation.

Animals↗
PubMed1992

Differential IgG avidity to rubella virus structural proteins.

Avidity maturation of IgG antibody responses directed against the structural proteins of rubella virus (E1, E2, and C) as well as whole rubella virus (RV) was assessed at sequential time intervals in 7 individuals following serologically confirmed wild rubella infection. Individual structural proteins were purified from tissue culture supernatants by differential centrifugation, followed by preparative SDS-PAGE under non-reducing conditions. Avidity of IgG anti-rubella responses was measured by using the 8 M urea elution technique and results expressed as an elution ratio [ER(%)]. A low mean ER(%) of 23% was determined for E1-specific IgG responses during the 10-20 day period following onset of clinical rubella, with subsequent maturation of avidity ER(%) values to 52%, 75%, and 84% at 3 months, 1 year, and 2 years, respectively, post-rubella. In contrast, IgG anti-E2 responses showed minimal avidity maturation with ER(%) values of 20%, 29%, 30%, and 31% over the same time intervals. Similarly, responses to the capsid protein (C) remained at low avidity ER(%) values of 21%, 29%, 36%, and 35% over the 2 year follow-up period. The avidity maturation values for IgG directed against whole RV preparations paralleled observations for E1-specific responses with ER(%) values of 23%, 52%, 85%, and 87%, respectively. These data support the need to assess individual protein-specific antibody avidities in order to more fully understand viral-specific immune responses.

Antibodies, Viral↗
PubMed1970

Studies on the regulation of avidity at the level of the single antibody-forming cell. The effect of antigen dose and time after immunization.

The hemolytic plaque formation of cells producing antibody against heterologous albumins was tested for sensitivity to specific inhibition by free antigen. The inhibition characteristics of plaques in this system were found to be a measure for the avidity of the antibody produced by the plaque-forming cells (PFC:s). High avidity-producing PFC:s were more sensitive to inhibition than low avidity PFC:s. Immunization with a high dose of antigen induced PFC:s that produced antibody with a lower avidity as compared to PFC:s from animals immunized with a low dose. The avidity was increased with time. Determinations of avidity at the serum level were also made, and the results were in agreement with the findings at the cellular level. The present method made it possible to demonstrate differences in avidity of antibody at the level of the single antibody-forming cell. It may also constitute a useful tool for the analysis of the cellular events leading to the production of antibodies with varying affinities during the immune response.

Animals↗