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PubMed1960

Gamma globulin and antibody formation in vitro. I. Gamma globulin formation in tissues from immature and normal adult rabbits.

Gamma globulin formation in vitro by various tissues was studied using the incorporation of C(14)-L-lysine into a protein precipitable by a specific anti rabbit gamma globulin serum prepared in a sheep. It was demonstrated that the rate of gamma globulin formation in similar numbers of spleen cells is much higher if taken from an immunized rabbit at the height of antibody formation than that in normal spleen cells. Besides spleen, other tissues shown to form gamma globulin in normal adult rabbits were: peripheral lymph nodes, bone marrow, lung, mesenteric lymph nodes, appendix, and thymus. In tissues from newborn rabbits gamma globulin formation could not be demonstrated. Rabbits 1 week old already showed a beginning of significant gamma globulin formation in appendix tissue, followed approximately 3 weeks later by gamma globulin synthesis in spleen and thymus. Histological observations on these tissues were described and correlated with findings on gamma globulin formation. In the discussion an attempt has been made to relate these observations on newborn and immature rabbits to those available in the literature on antibody formation in newborn animals.

Animals↗
PubMed1975

B cell tolerance induced by polymeric antigens. III. Dissociation of antibody formation and memory generation in tolerant mice.

Hapten (2,4-dinitrophenyl (DNP))-substituted type 3 pneumococcal polysaccharide (DNP-lys-S3) effectively suppresses both primary and secondary anti-DNP antibody responses to DNP-proteins. The present experiments show that tolerizing doses of DNP-lys-S3 have much less effect on B cell memory (re)generation in three distinct situations: (i) in serial transfers of DNP-protein-primed cells, (ii) in virgin mice tolerized before priming with DNP-hemocyanin, and (iii) in tolerized, hemocyanin-primed mice boosted with DNP-hemocyanin. Under some conditions tolerized mice developed 10-50% of normal memory in the absence of significant antibody formation. Isoelectric focusing analyses revealed that many B cell clones proliferate in tolerant mice, but produce very little antibody until transferred to further hosts. Clones that escape suppression in partially tolerant mice do not appear to be resistant to DNP-lys-S3, when retested. Since there is independent evidence that the generation of B memory cells is less T cell-dependent than the development of antibody-forming cells, these data are best explained by assuming that DNP-lys-S3 blocks lymphocyte cooperation. This would be expected to preferentially suppress antibody formation, and to spare memory generation.

Adoptive Transfer↗
PubMed2005

Major role of local immune responses in antibody formation to factor IX in AAV gene transfer.

The risk of an immune response to the coagulation factor IX (F.IX) transgene product is a concern in gene therapy for the X-linked bleeding disorder hemophilia B. In order to investigate the mechanism of F.IX-specific lymphocyte activation in the context of adeno-associated viral (AAV) gene transfer to skeletal muscle, we injected AAV-2 vector expressing human F.IX (hF.IX) into outbred immune-competent mice. Systemic hF.IX levels were transiently detected in the circulation, but diminished concomitant with activation of CD4+ T and B cells. ELISPOT assays documented robust responses to hF.IX in the draining lymph nodes of injected muscle by day 14. Formation of inhibitory antibodies to hF.IX was observed over a wide range of vector doses, with increased doses causing stronger immune responses. A prolonged inflammatory reaction in muscle started at 1.5-2 months, but ultimately failed to eliminate transgene expression. By 1.5 months, hF.IX antigen re-emerged in circulation in approximately 70% of animals injected with high vector dose. Hepatic gene transfer elicited only infrequent and weaker immune responses, with higher vector doses causing a reduction in T-cell responses to hF.IX. In summary, the data document substantial influence of target tissue, local antigen presentation, and antigen levels on lymphocyte responses to F.IX.

Adenoviruses, Human↗
PubMed1950

Experimental hypersensitivity in the rabbit; effect of inhibition of antibody formation by X-radiation and nitrogen mustards on the histologic and serologic sequences, and on the behavior of serum complement, following single large injections of foreign Proteins.

X-radiation and nitrogen mustard administration inhibit the formation of precipitins for whole bovine serum and bovine serum gamma globulin in the rabbit. When specific antibody formation is inhibited by these agents, intravenous injection of a single large dose of bovine serum gamma globulin is not usually followed by the development of tissue lesions 9 to 11 days later, as occurs fairly regularly in control animals. A fall in titre of serum complement to very low levels for 3 to 5 days is closely correlated in time with the disappearance of antigen from the circulation following the intravenous injection of single large doses of bovine serum albumin and bovine serum gamma globulin. A rise in complement titre to normal levels occurs as antibodies appear in the serum. This sudden fall in complement titre is correlated with the development of characteristic lesions, and does not occur when antibody formation is inhibited. The data presented are interpreted as evidence in favor of the concept that the lesions are due to a reaction between antigen fixed in or on tissue cells and circulating antibody. The possible significance of serum complement in the pathogenesis of anaphylactic tissue lesions is discussed.

Anaphylaxis↗
PubMed1984

The adjuvant activity of nonionic block polymer surfactants. II. Antibody formation and inflammation related to the structure of triblock and octablock copolymers.

We tested the ability of 17 surface-active agents to enhance antibody formation and inflammation. The surfactants were all block copolymers of hydrophilic polyoxyethylene (POE) and hydrophobic polyoxypropylene (POP), which differed in m.w. and mode of linkage of POP to POE. Mice were injected in each rear footpad with 1.25 mg of each surfactant with 25 micrograms of bovine serum albumin in an oil-in-water emulsion. Each agent produced a distinct pattern of immune response and inflammation. Preparations that are large and insoluble with the POE chains flanking the POP chains were very effective adjuvants for increasing antibody formation. They also activated complement and induced the release of chemotactic factors from serum. Increasing the percent of POE decreased adjuvant activity and inflammation. Decreasing the m.w. of the molecules while maintaining the proportions of POP and POE decreased the adjuvant activity and increased inflammation. Preparations synthesized in the reverse order, with the POP flanking POE, tended to induce granulomas instead of antibody. These data demonstrate that block copolymer surfactants have a spectrum of biologic activities that depend on the size and arrangement of their constituent parts. We suggest that much of the activity of these agents derives from their ability to form adsorptive surfaces similar to those of a mycobacterial glycolipid, quartz, and monosodium urate.

Adjuvants, Immunologic↗
PubMed1975

The influence of cyclophosphamide on antibody formation in the mouse.

A single injection of cyclophosphamide (CY) (300 mg/kg) 8 h prior to immunization results in a complete suppression of the antibody formation in mice. The effect of CY on the number and activity of the surviving cells in the lymphoid organs was studied. For all organs tested there was a decrease in cell numbers to 10% or less till day 3, followed by an increase in cell numbers in bone marrow, spleen and lymph nodes. The increase in cell numbers in the thymus was delayed till after day 11. The bone marrow reached normal levels on day 7. The spleen surpassed the normal levels on day 11, reaching cell numbers which were 50% over the normal ones. For the thymus cells this was found only on day 21. The numbers of lymph node cells remained low and reached normal levels or higher only when the mice were stimulated after CY treatment. This effect of stimulation was further seen in the spleen cell numbers, where after stimulation with antigen in Freund's complete adjuvant (FCA) or only FCA cell numbers of 200% of normal values were obtained. The suppression of antibody formation by CY could be restored by cells from spleen, lymph nodes, Peyer's patches or thymus and bone marrow, indicating a defect in both B and T cells caused by CY treatment. The target cell of CY treatment was studied by reconstitution of anergic mice with spleen or lymph node cells of CY treated mice with or without addition of normal bone marrow and thymus cells. This revealed that although the B cells is the main target cell of CY action, the impact on the T cell population is also considerable. When however CY treatment is followed by antigenic stimulation, there is a steep increase in the activity of the lymph node cells when bone marrow cells are added. This phenomenon resembles the education of thymus cells in the spleen of lethally irradiated mice in the presence of antigen.

Animals↗
PubMed1980

The specificity of antibody formation in mice following immunization with hapten-carrier complexes mixed with the surfactant, dimethyl dioctadecyl ammonium bromide.

Mice were immunized i.c. with various enlarged haptens conjugated to bovine serum albumin and mixed with the cationic, surface active lipid, dimethyl dioctadecyl ammonium bromide (DDA). This immunization generated delayed-type hypersensitivity (DH) in these mice without detectable concomitant antibody formation. The DH was measured as footpad swelling. However, both direct and indirect hapten-specific PFC could be detected in peripheral lymph nodes and in spleens 4 days after a challenge injection. Although the adjuvant, DDA, promotes a strong cross-reactivity in DH between heterologous hapten-carrier complexes, the antibody-forming cells produced 4 days after challenge showed relatively high specificity for the immunizing hapten. This indicates only weak cross-reactivity at the antibody-forming cell level co-existent with high cross-reactivity in DH expression to the same hapten-carrier complexes. These results are consistent with the possibility that B-cell receptors may be capable of expressing a greater degree of hapten specificity than T-cell receptors. It is tentatively concluded that Thelper cells participating in antibody formation may represent a subset of the T cells involved in DH.

Animals↗
PubMed1988

Oligonucleotide linked to human gammaglobulin specifically diminishes anti-DNA antibody formation in cultured lymphoid cells from patients with systemic lupus erythematosus.

In vitro studies were undertaken to determine whether the level of anti-DNA antibody can be modulated in humans with systemic lupus erythematosus (SLE). DNA fragments of different sizes, i.e., oligonucleotide (N20-30) or oligonucleotide (N10-100), were covalently linked either to human gammaglobulin (HGG) and used as tolerogens or to keyhole limpet hemocyanin and used as immunogens. Experiments were done to determine whether such tolerogens specifically diminish antibodies to denatured DNA, native DNA, or both. PBL were obtained from 87 patients with SLE, 55 of whom spontaneously produced anti-DNA antibodies in vitro. Furthermore, of these 55 test subjects 23 made anti-DNA antibodies in response to antigen challenge in vitro. Exposure of PBL to tolerogenic oligonucleotide-HGG reduced spontaneous antibody formation in 34 of the 55 patients' PBL and abrogated the in vitro-induced response in all instances. The suppression was tolerogen specific. In some SLE patients lymphoid cells were suppressed by both (N10-100)-HGG and (N20-30)-HGG, while in others lymphoid cells were suppressed by only one. Longitudinal studies of spontaneous antibody production showed that the same tolerogens consistently reduced anti-DNA antibody formation in lymphoid cells of 12 patients on several occasions over a 2-yr interval, but in 8 others the results were either variable or inconsistent. In contrast, tolerogens consistently abrogated the antigen-induced response in all 23 patients' PBL. These results obtained in humans in vitro suggest that the principle of carrier-determined tolerance could be applied as a specific therapy for SLE in vivo.

Antibodies, Antinuclear↗
PubMed1993

The regulation of T cell-dependent antibody formation in vitro by CD40 ligand and IL-2.

Our study demonstrates the central role for the murine CD40 ligand and IL-2 in contact-dependent T cell help for Ag-specific primary antibody responses in vitro. Helper T cell clones were found to express CD40 ligand after activation with CD3 mAb. Membrane-bound recombinant CD40 ligand expressed on fixed CV1/EBNA cells had similar B cell-activating properties as T cell clones that had been activated and then fixed. These activities include the induction of B cell proliferation, induction of polyclonal secretion of multiple Ig isotypes in a cytokine-dependent manner, and induction of Ag-specific antibody responses by purified B cells. The induction of polyclonal Ig secretion by the recombinant CD40 ligand required IL-4 and IL-5 although optimal Ag-specific antibody formation required IL-2. Finally, soluble CD40.Fc inhibited the induction of Ag-specific antibody responses by fixed, activated Th cell clones. The requirement for both CD40 ligand and IL-2 for induction of Ag-specific antibody responses was mediated, in part, by the induction of B cell IL-2R expression by CD40 ligand. We conclude that the interaction of CD40 on B cells with its ligand on activated T cells is an integral event in the early activation of B cells to grow and differentiate to antibody formation.

Animals↗
PubMed1986

Suppression and enhancement of humoral antibody formation by herpes simplex virus types 1 and 2.

Intraperitoneal infection of mice and rats by herpes simplex virus type 2 (HSV-2) but not type 1 (HSV-1) resulted in suppression of antibody formation on subsequent challenge with HSV-1 or HSV-2. Application of silica considerably enhanced antibody formation after primary HSV-1 infection, but only slightly after primary HSV-2 infection. Suppression induced by HSV-2 was, however, reduced significantly by injection of silica 21 days later, on the day of the second injection of HSV-2. Suppression could be detected soon after infection by HSV-2. The degree of this suppression depended on the dose of the injected virus and was abolished by u.v. irradiation of the virus prior to inoculation. Likewise the weak antibody response induced by HSV-2 was abolished for both neutralizing and ELISA antibodies. Infections with HSV-1 evoked considerable numbers of HSV-specific antibody-producing B cells, when assessed by an enzyme-linked immunospot assay. The B cell response to HSV-2, however, was very weak. Silica considerably enhanced the number of specific antibody-producing B cells only during primary HSV-1 infections. The present results in combination with earlier data demonstrate the central role of macrophages, which seem to be the primary target affected by silica, for enhancement and suppression of HSV-induced antibody generation.

Animals↗
PubMed1975

Local antibody formation within the eye: a study of immunoglobulin class and antibody specificity.

Primary immunogenic uveitis was induced in the rabbit eye with a single injection of antigen into the vitreous, and secondary booster uveitis responses were induced two months later by intravenous administration of the same antigen. The distribution of immunoglobulin classes and the specificity of the antibodies produced were assessed early and late in the primary response and early and late in the secondary response, and were compared with the analogous responses in the spleen and regional lymph nodes. At each of these stages of intraocular antibody response, IgG formation was higher and IgM formation lower than that seen in organized lymphoid tissues, while the proportion of IgA-forming cells was similar to the low levels usually found in the spleen. A significant proportion of IgA-forming cells was found in the perilimbal conjunctiva, and even greater levels in the lacrimal glands. At each stage of the response, the proportion of immunoglobulin-forming cells making antibody specific for the inciting ovalbumin antigen was surprisingly low, reaching only seven per cent during the late primary reaction and 18 per cent during the late secondary reaction.

Animals↗
PubMed1985

A 3 beta-cholestanyl-containing mono-benzylpenicilloyl oligoamide and peptide suppress anti-benzylpenicilloyl antibody formation in mice.

A long-chain linear mono-benzylpenicilloyl (BPO) oligoamide and a succinoylated mono-BPO decalysine were tested in BALB/c mice for suppression of IgE and IgG1 antibody formation. Both compounds were available with either a free C-terminal end or were C-terminally linked to a hydrophobic 3 beta-cholestanyl residue. Only the sterol-containing derivatives suppressed hapten-specific IgE and IgG1 responses. Substantial suppression was obtained when the compounds were administered before primary or secondary, but not later immunizations. In an adoptive cell transfer experiment, spleen cells from tolerized animals actively suppressed anti-BPO IgE antibody formation of immune spleen cells. This effect was reversed by pretreatment of the tolerized spleen cells with anti-Lyt-2.2 antibody plus complement. The requirement for macrophages in the induction of T suppressor cells was demonstrated by injecting antigen-pulsed macrophages into naive recipients; upon immunization, only mice treated with tolerogen-pulsed macrophages showed suppressed anti-BPO IgE responses. It is suggested that lipid modification of antigens alters their processing and presentation by macrophages in a manner that leads to the induction of T suppressor cells. Injection of the cholestanyl derivatives into passively sensitized guinea pigs elicited anaphylactic reactions. By immune precipitation analysis and molecular weight estimation, these derivatives were shown to form micelles in aqueous solution. Therefore, the anaphylactic response appeared to be due to their behavior as multivalent antigens.

Anaphylaxis↗
PubMed2003

Comparison of bovine and porcine heparin in heparin antibody formation after cardiac surgery.

BACKGROUND: Heparin-induced thrombocytopenia (HIT) is a potentially devastating complication of heparin therapy. The incidence of clinical HIT after cardiovascular surgery is less than 2%, although asymptomatic antibodies to heparin-platelet factor 4 (PF4) occur more frequently. Bovine heparin is thought to cause more HIT than porcine heparin, although this has never been established for heparin use during coronary artery bypass grafting. We therefore undertook a randomized, prospective study of heparin-PF4 antibody formation in patients undergoing first-time CABG given intraoperative bovine or porcine heparin. METHODS: Two hundred seven patients (108 porcine, 99 bovine) completed the study. Heparin given pre- or postoperatively was always porcine. Platelet counts and heparin-PF4 antibody tests (enzyme-linked immunosorbent assays) were performed preoperatively and daily until postoperative day 7 or discharge if earlier. RESULTS: The overall incidence of heparin-PF4 antibody formation was 42%. Six patients (2.9%) were positive preoperatively, of which, 1 developed clinical HIT. When these were excluded, seroconversion rates were 44 of 99 (44.4%) and 33 of 108 (30.6%) for bovine and porcine heparin, respectively (p = 0.041). Among patients who produced antibodies, most (90% bovine, 85% porcine) seroconverted after postoperative day 2. There were no differences in postoperative platelet counts; only 1 patient developed thrombosis associated with seroconversion, but without developing thrombocytopenia. The seroconversion rates for patients having cardiopulmonary bypass or off-pump surgery were not significantly different. CONCLUSIONS: This study confirms the high frequency of heparin-PF4 antibodies after coronary artery bypass grafting and demonstrates a significantly higher incidence after bovine heparin. However, because some patients may seroconvert after discharge, our study may underestimate the true incidence.

Animals↗
PubMed2002

Antibody formation during intravenous and intramuscular therapy with Erwinia asparaginase.

BACKGROUND: Determination of the frequency of antibody formation during first and second exposure to Erwinia asparaginase after i.v. and i.m. administration. PROCEDURE: Thirty-nine children with newly diagnosed acute lymphoblastic leukemia (ALL) were included in this prospective study. Antibodies were determined (ELISA method) in plasma from these patients on specific days during and after therapy with 30,000 IU/m(2) i.v. or i.m. every day for ten days during the induction phase (first exposure). For 19 children, antibodies were measured in plasma during and after the re-induction phase (second exposure) following treatment with 30,000 IU/m(2) i.v. or i.m. twice a week for two weeks (Mondays and Thursdays). On the same days of therapy, enzyme activity (spectrophotometric method) and the concentration of asparagine (HPLC) was determined. RESULTS: During the first exposure, none of the patients developed anti-Erwinia asparaginase antibodies. During the second exposure, one patient (1 of 8 patients) treated intravenously developed antibodies, which were associated with disappearance of enzyme activity and reappearance of asparagine. Three of eleven patients developed antibodies of pharmacokinetic importance after i.m. therapy. None of the children had any clinical symptoms of hypersensitivity. CONCLUSIONS: The formation of antibodies and subsequently altered pharmacokinetics of Erwinia asparaginase seemed to be of importance only during a second period of asparaginase therapy.

Adolescent↗