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PubMed1994

[Dynamics of antibody formation, isotypes and specificity of antibodies in the immune response of Balb/c mice to cytochrome c].

The production of IgG antibody (Ab) to cytochrome c in BALB/c mice reached its maximum four weeks after primary immunization which is significantly later than the response to the same dose of keyhole limpet hemocyanin (KLH). The relative amounts of IgG subclasses varied during the immune response to KLH: IgG2a Abs dominating on day 11 were replaced by IgG1 on day 30 after immunization. This was not the case with anti-cytochrome c Abs: their IgG subclasses varied significantly among individual mice within the strain. The heme elimination altered the cytochrome c antigenic structure, although some antigenic determinants remained intact. The heme with its neighbouring residues represented by heme peptide 14-22 was not recognized by anti-cytochrome c Abs. Serum IgG Abs interacted with peptides 1-65 and 1-80 obtained by BrCN hydrolysis of cytochrome c; however, they did not bind to peptide 66-104. The Abs affinity purified on cytochrome c bound to peptides 1-65 and 1-80, while the Abs purified on peptide 1-65 or apo-cytochrome could recognize native cytochrome c as well.

Animals↗
PubMed1979

Effect of levamisole on the auto-antibody formation in nude mice.

The effects of levamisole on the formation of antibody to double-stranded DNA (ds-DNA), an auto-antibody, and to some thymus-dependent antigens were studied in nude (nu/nu) mice. The antibody titre to ds-DNA in nu/nu mice treated with levamisole was lower than that in control animals. The number of Thy-1-antigen-positive (Thy-1+) cells in the spleen from nu/nu mice treated with levamisole was higher than that from non-treated animals. It is suggested that the Thy-1+ cells were induced by levamisole in nu/nu mice and these cells suppressed the formation of antibody to ds-DNA, whereas the formation of antibody to a DNP-conjugate (OVA) and SRBC, thymus-dependent antigens, was not evoked in nu/nu mice after the treatment with levamisole.

Animals↗
PubMed1981

[The cybernetic circuit of the regulation of antibody formation].

The current theory concerning the formation of antibodies is no more sustainable against the recent view on the formation of complex structures, that involves, together with a random variability, also an ordered variability derived from information interactions. This paper aims at showing that the formation of antibodies requires the existence of a complex sensor which can be excited by the presence of antigenic structures of any shape. The stimulation of this sensor originates both a mass type feedback and a form type feedback; the latter consisting in the activation of a conformational genetic variability that turns into a form variability of the immunoglobulinic active site. This site can thus take a form capable to react with the antigen. The reaction with the antigen acts back negatively upon the sensor and causes the permanent acquisition in repertory of the active form for the subsequent disappearance of the form variability in the immunoglobulinic active site.

Animals↗
PubMed1994

Effects of peptone on hybridoma growth and monoclonal antibody formation.

Hybridoma WuT3 secreting a monoclonal antibody against T lymphocytes was grown in RPMI 1640 medium supplemented with 1% human serum. The effect of the concentration of peptone, as an additive, was investigated on cell growth, monoclonal antibody formation, and cell metabolism over 0-10 g l-1 range. It was found that 1-5 g l-1 peptone can significantly promote the growth of cells and increase the formation of monoclonal antibody, especially at 3-5 g l-1, when both the accumulating level and secretion rate of monoclonal antibody are higher than that at other peptone concentrations. Based on glucose, lactate and ammonia analysis data, the efficiency of glycolysis was assessed and the utilization of amino acids was more efficient at 3-5 g l-1 peptone. The cell growth and monoclonal antibody formation were inhibited at higher peptone concentrations, e.g. 10 g l-1.

Amino Acids↗
PubMed1983

Kinetics and genetics of herpes simplex virus-induced antibody formation in mice.

The kinetics of antibody synthesis was investigated after intraperitoneal, subcutaneous, and footpad infection of various strains of mice with herpes simplex virus. Immunoglobulin M antibodies appeared 5 days after and immunoglobulin G antibodies appeared 10 to 12 days after intraperitoneal infection with herpes simplex virus type 1. The major histocompatibility complex and the background genome of inbred mice were not found to have a systematical influence on antibody synthesis. Female mice, however, consistently produced more antibodies than did male if the infection was done intraperitoneally, but not if it was done subcutaneously or into footpads. Castration considerably increased the amount of antibodies produced by male mice. The difference in antibody formation between females and males could be abolished by injection of silica; moreover, antibody titers were enhanced by this treatment. This has also been found by immunization with a Formalin-inactivated herpes simplex virus vaccine. The effect of silica in enhancing antibody formation could be observed up to 12 days after infection. Infectious virus could be detected up to 2 days after infection, and herpes simplex virus type 1 antibody-stimulating antigens could be detected up to 4 days in ultrasonicates of macrophages. The assumption is made that androgen-sensitive cell populations, including macrophages and their soluble products, are involved in antibody-depressing mechanisms.

Animals↗
PubMed1968

The effect of antigenic competition on various manifestations of humoral antibody formation and cellular immunity.

The effect of antigenic competition on various parameters of humoral antibody formation and cellular immunity was studied in mice. Several pairs of antigens were employed in the investigation of the competitive aspects of induction of humoral antibody formation. Induction of a primary immune response to hemocyanin in Swiss white female mice moderately suppressed the induction of both 19S and 7S antibody formation to goose or rat erythrocytes. Suppression of 7S antibody formation was maximal when a time interval of 1-3 days separated the sequence of injections, although suppression was noted for intervals of up to 14 days. The induction of a primary immune response to rat RBC, the second of the two antigens in sequence, also suppressed The induction of both 19S and 7S antibody formation to goose RBC when appropriate intervals of 1-3 days were employed between injections. The induction of a secondary immune response to rat RBC totally suppressed the primary induction of both 19S and 7S antibody formation to goose RBC administered in the appropriate time sequence. Subsequently, it was shown that the secondary immune response to the suppressed antigen (goose RBC) elicited 30 days after induction of a primary immune response (5 days after secondary immunization with rat RBC) was characterized by deficient 19S and 7S antibody production. These levels were suppressed even in comparison with a normal primary immune response to this antigen. The results were interpreted in part on the basis of a deficiency of formation of primed cells associated with immunological memory. Alternatively, evidence was obtained for the development of a split type of immunological tolerance in 6 of 10 animals studied, since a total suppression of 7S antibody production was obtained in association with deficient 19S antibody synthesis (titers < 1/10). The induction of a primary immune response to several antigens in A/J female mice suppressed the processes of cellular immunity as manifested by prolonged survival of skin grafts from C57 BL/6J female donors. These results were interpreted as evidence for the existence and utilization of processing cells by the initial immune stimulus yielding a deficiency of cells available for processing the second antigen administered in sequence.

Animals↗
PubMed1986

Cyclosporin A-induced suppression of ongoing IgE antibody formation in the mouse.

Persistent anti-ovalbumin (OA) IgE antibody formation in the mouse was suppressed by oral administration of cyclosporin A (Cy A). Spontaneous anti-OA IgE antibody formation in vitro was also suppressed by Cy A added to the culture. Anti-OA IgG antibody responses in vivo and in vitro were less affected by Cy A. Cy A-induced immunosuppression was T cell-dependent since removal of T cells from the immune spleen cell suspension abolished the Cy A-induced suppression of antibody formation. Supplementing normal spleen T cells resulted in recovery of Cy A-induced suppression of spontaneous antibody formation in vitro. Cy A-induced suppressor T cells carried both Lyt 1 and Lyt 2 surface markers.

Animals↗
PubMed1978

Antibody formation to double-stranded DNA in nu/nu and nu/+ mice.

Antibody formation to double-stranded (ds-) DNA in nude mice (nu/nu) and normal littermates (nu/+) was studied using a Millipore filter method. The mean antibody titre to ds-DNA in the sera of nu/nu mice was generally higher than that in nu/+ mice raised in the same environment. However, in both genotypes, anti-ds-DNA titres varied according to the environmental condition in which the animals were raised. Mice maintained germ-free showed no significant antibody formation to ds-DNA. Nu/+ thymus and spleen cells passively transferred to nu/nu mice reduced the antibody titre to ds-DNA in the recipients. Immunochemical studies indicated that the antibodies to ds-DNA were IgM. It is suggested that T cell-mediated regulatory mechanisms control antibody formation to ds-DNA and that some infections trigger antibody formation to ds-DNA.

Animals↗
PubMed1990

Antimurine antibody formation following OKT3 therapy.

OKT3 is an IgG2a murine monoclonal antibody directed against the CD3 antigen receptor of human T lymphocytes. A major concern with OKT3 treatment in solid organ transplant recipients is the development of antimouse antibody, which may preclude retreatment with this agent. We have administered OKT3 on 215 occasions (150 renal, 34 hepatic, 26 cardiac, 5 pancreatic) in 179 patients between April 1982 and December 1988. The mean duration of treatment was 10.5 days (range, 2-22 days). Antimouse antibody data were analyzed on the most recent 133 treatment courses where the antibody status was available pretreatment. Determination of antimouse antibody production was elicited by ELISA technology at days 0, 7, 14, and 28 of OKT3 treatment. Patients were categorized according to the antibody response as follows: (a) absence of antibody; (b) low titer (1:100); or (c) high titer (greater than or equal to 1:1000). Our earlier experience has demonstrated that retreatment with OKT3 is successful in groups a and b. The development of antimurine antibodies was analyzed with regard to the following parameters: (1) The duration of OKT3 treatment; (2) treatment type (prophylactic, primary, or secondary); (3) primary treatment or retreatment; (4) concomitant immunosuppressive regimen (double or triple therapy); (5) dosage of concomitant immunosuppressive drugs; and (6) transplant organ type. The following results were obtained. (1) Duration of treatment had no effect on antibody production (11.0 days in antibody negative and 10.0 days in antibody positive). (2) There was no difference in antibody formation rates for the first treatment of OKT3 when it was used as prophylaxis (26%), primary (19%), or secondary (27%) therapy. (3) Antibody formation rate with first treatment was 29%; with retreatment, patients who were antibody negative following first treatment became positive in 28% of cases, and retreated patients who were low titer positive following first treatment converted to high titer in 57% of cases. (4) Antibody formation was higher in patients receiving double immunosuppressive therapy (36%) than in those receiving triple immunosuppressive therapy (21%) during OKT3 treatment. (5) Concomitant immunosuppression was lower in the antibody-positive group during OKT3 therapy: steroids, 61 mg/day vs. 52 mg/day; azathioprine, 89 mg/day vs. 66 mg/day; CsA, 317 mg/day vs. 186 mg/day. (6) Antibody formation rates were lower in non-renal transplants following first treatment with OKT3 (liver 17%, heart 17%, kidney 28%); this reflects the higher doses of concomitant immunosuppressive therapy used in nonrenal transplants.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1975

The mode of action of mycobacterial adjuvants. III. The clonal nature of antibody formation and the effect of mycobacterial adjuvant on antibody-forming cell clones.

Localization of 19S and 7S plaque forming cells detected by Jerne plaque technique were examined in the spleens of irradiated recipient mice transferred with a limiting number of spleen cells and SRBC. All the plaques within a single colony were homogeneous in size and appearance. This supports the clonal nature of antibody formation. An addition of a mycobacterial adjuvant, wax D, to the sensitizing antigen, SRBC, caused an increase in the number of clones (colonies) developing large plaques. It is suggested that there may be normally available competent precursors for clones developing large plaques and the precursors may specifically increase in number in the presence of the adjuvant.

Adjuvants, Immunologic↗
PubMed1984

Effect of vitamin E on IgE antibody formation in mice.

Effect of vitamin E (alpha-tocopheryl acetate and alpha-tocopheryl nicotinate) on IgE antibody formation in mice was investgiated . Female BALB/c mice were immunized with dinitrophenylated ascaris protein (DNP-As) and aluminium hydroxide gel (alum). Supplementation of vitamin E in diets or oral administration of vitamin E mixed with sesame oil resulted in a suppression of IgE antibody formation. On the contrary to IgE antibody formation, IgM or IgG (hemagglutinin; HA) formation was significantly enhanced. These results indicate that vitamin E is capable of suppressing IgE antibody formation and enhancing non-IgE antibody formation.

Administration, Oral↗