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At least 145 records · Page 8Linked to original sources
PubMed1971

Antibody formation: reduced responses after administration of excessive amounts of nonspecific stimulators.

Enhancement of antibody formation in vitro and in vivo by poly(A.U), cyclic AMP, dibutyryl cyclic AMP, or any one of these agents in combination with theophylline or caffeine, is usually limited to certain dose ranges. High doses of these nonspecific stimulators can produce less or no enhancement, or may actually inhibit antibody formation. Such dose-response relationships may be pertinent to an understanding of phenomena of specific immunological nonresponsiveness and certain types of antigenic competition.

Animals↗
PubMed1994

Genetic control of the radiosensitivity of lymphoid cells for antibody formation ability in mice.

To analyze the genetic basis of the relationship between the radiosensitivity of the immune response and radiation lymphomagenesis, we examined the radiosensitivity of lymphoid cells for antibody formation in BALB/cHeA, STS/A, F1 hybrids, and their recombinant inbred mouse strains. The decrease in the number of plaque-forming spleen cells in BALB/cHeA mice exposed to 3 Gy X-irradiation was more than tenfold that in STS/A mice. The phenotype of radioresistance was dominant over sensitivity. The coincidence between the strain distribution patterns of the genetic markers and radiosensitivities of antibody formation in the various recombinant inbred strains was in the region with the Igh locus on chromosome 12. There was obvious difference between the patterns in the region containing the Ifa locus on chromosome 4 which has been shown to be related to the incidence of radiation-induced lymphomas. These results indicate that the region on chromosome 12 may contain major gene(s) related to radiosensitivity for antibody formation.

Animals↗
PubMed1985

Bovine herpesvirus-1 infection of cattle: kinetics of antibody formation after intranasal exposure and abortion induced by the virus.

The kinetics of antibody formation in Holstein heifers after primary and secondary intranasal inoculation of bovine herpesvirus-1 (BHV-1) and after BHV-1-induced abortion was determined. Sera were fractionated by gel filtration and ion-exchange chromatography. The antibody activity within serum immunoglobulin (Ig) isotypes was assessed, using a plaque-reduction neutralization assay. The primary immune response to BHV-1 infection was characterized by the appearance of IgM and IgG antibodies in serum by postinoculation day (PID) 7. Maximal IgG antibody activity occurred at PID 35 in nonpregnant heifers and at PID 14 in pregnant heifers. Thereafter, IgG antibody activity declined slowly in both groups of heifers. Maximal IgM antibody activity occurred at PID 14 in both groups of heifers and declined rapidly thereafter. The IgG antibody activity during primary immune responses was restricted to the IgG1 subclass. Secondary responses were characterized by anamnestic IgG antibody responses. Antibody activity was present within the IgG1 and IgG2 subclasses during secondary immune responses, but the increase in antibody activity during this period was primarily in the IgG2 subclass. Secondary IgM antibody formation was elicited by abortion induced by the intra-amniotic inoculation of BHV-1, but not by reexposure by the intranasal route. Abortion occurred in 1 heifer 28 days after intranasal BHV-1 inoculation. Abortion in this heifer was not associated with a secondary antibody response. The nature of BHV-1 antigenic exposure in the bovine determined the relative distribution of anti-BHV-1 antibody activity in serum IgM, IgG1, and IgG2. The formation of IgM antibody, with the exception of secondary intranasal exposure, indicated recent BHV-1 antigenic exposure.(ABSTRACT TRUNCATED AT 250 WORDS)

Abortion, Veterinary↗
PubMed1985

Kinetics of antibody formation after the reactivation of bovine herpesvirus-1 infection in cattle.

Holstein heifers previously infected with bovine herpesvirus-1 were treated with corticosteroids to reactivate latent infection. The kinetics of serum immunoglobulin (Ig) M, IgG1, and IgG2 antibody formation were determined. The secondary immune response which developed as a consequence of virus reactivation was characterized by an anamnestic IgG antibody response. Secondary IgG1 and IgG2 antibody formation constituted the IgG antibody response. In addition, secondary IgM antibody formation was elicited by this form of bovine herpesvirus-1 antigenic exposure.

Animals↗
PubMed1996

Preferential induction of a Th1 immune response and inhibition of specific IgE antibody formation by plasmid DNA immunization.

We compared the antigen-specific antibody isotypes and lymphokine secretion by CD4+ T cells in BALB/c mice immunized intradermally with either Escherichia coli beta-galactosidase (beta-gal) or plasmid DNA (pDNA) encoding beta-gal in a cytomegalovirus-based expression vector (pCMV-LacZ). pCMV-LacZ induced mainly IgG2a, whereas beta-gal in saline or alum induced IgG1 and IgE beta-gal-specific antibodies. In addition, splenic CD4+ T helper (Th) cells isolated from pDNA-immunized mice secreted interferon-gamma but not interleukin (IL)-4 and IL-5, whereas Th cells from beta-gal-injected mice secreted IL-4 and IL-5 but not interferon-gamma after in vitro stimulation with antigen. Together these data demonstrate that pDNA immunization induced a T helper type 1 (Th1) response, whereas protein immunization induced a T helper type 2 (Th2) response to the same antigen. Interestingly, priming of mice with pCMV-LacZ prevented IgE antibody formation to a subsequent i.p. beta-gal in alum injection. This effect was antigen-specific, because priming with pCMV-LacZ did not inhibit IgE anti-ovalbumin antibody formation. Most importantly, intradermal immunization with pCMV-LacZ (but not pCMV-OVA) of beta-gal in alum-primed mice caused a 66-75% reduction of the IgE anti-beta-gal titer in 6 weeks. Also, pCMV-LacZ induced specific IgG2a antibody titers and interferon-gamma secretion by Th cells in the beta-gal in alum-primed mice. The data demonstrate that gene immunization induces a Th1 response that dominates over an ongoing protein-induced Th2 response in an antigen-specific manner. This suggests that immunization with pDNA encoding for allergens may provide a novel type of immunotherapy for allergic diseases.

Animals↗
PubMedDate not supplied

[Immunocorrecting and protective effect of proteolytic enzymes on antibody formation in mice in staphylococcal infection and antibiotic treatment].

The impact of proteolytic enzymes on the humoral immune response, survival rate and mean survival time of mice, infected with S. aureus culture and receiving antibiotics was studied. Infection with staphylococcal suppressed the formation of antibodies to sheep red blood cells. Ampicillin made this immunosuppression even more pronounced, while gentamicin produced practically no effect on the degree of immunosuppression in the infected animals. Proteolytic enzymes terrilytin and terridecase exhibited immunocorrecting properties when used in combination with antibiotics. Terridecase, the immobilized form of the enzyme proved to have the highest activity. In experimental generalized staphylococcal infection all preparations under study produced a protective effect. The maximum effect was noted after the use of ampicillin in combination with terridecase.

Ampicillin↗
PubMed1976

Immune response in dog. 3. Antibody formation in dogs and rabbits to human serum proteins and keyhole limpet haemocyanin.

Antibody formation in dogs and rabbits to human serum proteins and keyhole limpet haemocyanin (KLH) following primary, secondary and multiple stimulation was analysed. Primary injection of human serum stimulates the formation of precipitin antibodies to beta2 lipoprotein in dogs, beta2 lipoprotein and beta globulin in rabbits. After a secondary dose the rabbits formed precipitins to a whole range of human serum proteins, while the dogs to beta2 lipoprotein, albumin, beta globulin. When the primary dose of antigen was divided over a period of 8 weeks, the dog produced precipitins to beta2 lipoprotein while the rabbit to a wide range of serum proteins. Secondary stimulation of these animals did not increase the number of precipitins formed. Quantitative analysis of the antibody produced show that the best response was with beta2 lipoprotein followed by albumin and beta globulin. As the immunogenicity of the antigen was greater the differences between the two species were narrow. These differences were less pronounced following the primary injection than after the secondary and multiple stimulations. The primary response to KLH (which represents mainly IgM) is better in the dog than in the rabbit, while the secondary response (IgG) was better in the rabbit. The poorer IgG response in the dog compared to the rabbit, observed in all the experiments, is discussed.

Animals↗
PubMedDate not supplied

Serum sperm agglutinating antibody formation in vasectomized men treated with dexamethasone.

The effect of immunosuppression with dexamethasone on sperm antibody formation following vasectomy in men was determined. Vasectomized men were treated with dexamethasone (4 mg) tablets starting two days prior to vasectomy and each day thereafter for a total of eight days for a total dose of 30 mg. There was no significant difference in serum sperm agglutinating antibody, cholesterol, triglycerides, or lipoproteins between the dexamethasone and placebo groups. The finding that immunosuppression at the time of vasectomy did not inhibit sperm antibody formation in man was surprising because in a similar study with Cynomoglus monkeys treatment at the time of vasectomy with dexamethasone inhibited sperm antibody development. The difference between the two studies may be that in monkeys sperm antigen presentation comes at the time of vasectomy and therefore immunosuppression at this time can prevent an immune response, but in man sperm antigen presentation comes at some later time following vasectomy. This species difference in sperm antigen presentation following vasectomy in man compared to monkeys may affect subsequent atherosclerosis development and explain why no cardiovascular disease is found in man following vasectomy.

Antibody Formation↗
PubMed1977

[Cellular and humoral indicators of antibody formation in rats with liver lesions caused by the antihepatocytotoxic serum].

As revealed, antihepatocitotoxic serum caused a sharp suppression of antibody genesis in rats at the early period (the 3rd day) after its 5 administrations; this was indicated by a marked reduction of the antibody-forming cell count in the spleen and reduction of the circulating antibody titres (hemolysins and hemagglutinins). Along with this, antibody formation was stimulated in the liver in the course of the whole month of study. By the end of the month suppression of antibody formation was replaced by its stimulation.

Animals↗
PubMed1964

HOMEOSTASIS OF ANTIBODY FORMATION IN THE ADULT RAT.

Passive immunization of rats with homologous anti-sheep erythrocyte serum markedly inhibited the primary antibody response to various doses of sheep erythrocytes. Inhibition was "specific" and apparently produced by either "19S" or "7S" antibody to the antigen. Passive immunization inhibited splenic hyperplasia associated with the primary antibody response. Passive immunization 24 hours after active immunization effectively inhibited the primary antibody response. The markedly suppressive effect of specific antibody on the primary antibody response contrasted sharply with the absence of this effect on the secondary response. Antigen-antibody complexes formed in vitro elicited no measurable primary antibody response but did elicit a high secondary response. Exposure of normal spleen cells to the antibody in vivo or in vitro suppressed their response to the antigen in x-irradiated recipients. In contrast, cells from previously immunized animals transferred to x-irradiated animals produced antibody in the presence of passively given antibody. Thus, "potential antibody-forming cells" from normal animals were unresponsive to the antigen in the presence of specific antibody, while "antibody-forming cells" from previously immunized animals responded to the antigen in the presence of antibody. Presumably, antibody actively produced in small quantities by a few antibody-forming cells might inhibit antibody formation by potential antibody-forming cells. Confirmation of this suggestion was obtained by showing that some animals initially injected with small doses of antigen failed to produce measurable antibody to subsequent injections of larger doses of the antigen. Low doses of antigen capable of inducing unresponsiveness produced no measurable circulating antibody, but these doses did produce increased numbers of plaque-forming (antibody-releasing) cells in spleens of rats. Thus, the formation of specific antibody may provide a homeostatic or "feed-back" mechanism which controls or limits production of specific antibody to the portion of the antibody-forming system previously stimulated by the antigen. This mechanism may account in part for immunological unresponsiveness produced in certain other related experimental systems.

Animals↗
PubMed1975

[The effect of the polyvalent proteinase inhibitor, trasylol, on antibody formation under normal conditions and in experimental atherosclerosis].

Antibodies to erythrocytes of sheep and human serum albumin were formed in rabbits with alimentary atherosclerosis as intensively as in control. Trasilol failed to affect the antibody formation in normal animals, but sharply decreased the production of specific immunoglobulins (especially the 7S) in rabbits with experimental atherosclerosis. Thus, the action of the preparation is realized not by way of direct inhibition of functional activity of the lymphoid tissue cells, but by inhibiting the immunostimulating factor circulating in the blood in experimental atherosclerosis.

Animals↗
PubMed1992

Influence of ageing on antibody formation in vivo after immunisation with the primary T-cell dependent antigen Helix pomatia haemocyanin.

The in vivo antibody response to the primary T-cell dependent antigen Helix pomatia Haemocyanin (HPH) was studied, in order to detect the possible presence of a humoral immune deficiency in ageing. The IgG subclass distribution of the specific antibodies was also determined. In order to define a dose of HPH which could be used to discriminate between the responsiveness of healthy and immunocompromised individuals, we first established a dose-response curve for this antigen in 60 healthy young volunteers. Their responses were compared with the responses of a group of patients suffering from end stage renal failure. The patients who were treated with haemodialysis showed a significantly lower IgM, IgG and IgA anti-HPH antibody response after immunisation with a dose of 30 micrograms HPH, which could be restored by increasing the antigen dose. Patients treated with continuous ambulant peritoneal dialysis and a group of elderly persons, selected according to the Senieur protocol, showed no impairment of antibody formation after immunisation with 30 micrograms HPH, but in the non-Senieur elderly the anti-HPH antibody response was significantly lower. Furthermore, Senieur and non-Senieur elderly persons showed a diminished IgG2 anti-HPH antibody formation, whereas in the elderly non-Senieur individuals and in the patients with renal insufficiency, IgG1 and IgG3 anti-HPH antibodies were also diminished. This study clearly shows that the so-called age-associated immune deficiency can be the result of disease and is not necessarily due to the ageing process itself.

Adult↗
PubMed1969

Cells involved in the immune response. VII. The demonstration, using allotypic markers, of antibody formation by irradiation-resistant cells of irradiated rabbits injected with normal allogeneic bone marrow cells and sheep erythrocytes.

Bone marrow cells obtained from rabbits of one allotype were injected into irradiated rabbits of a different allotype. The recipients were also injected with sheep red blood cells, and their spleen cells were tested for plaque-forming capacity 7 days later. Spleen cells of all recipients gave large numbers of plaques as did spleen cells incubated with antiserum, directed toward donor allotype. However, incubation of the recipient spleen cells with antiserum directed toward recipient allotype completely suppressed plaque formation. These results demonstrate that antibody-formation in irradiated recipients of transferred lymphoid cells is a property of the recipient animal and that the antibody-forming cell is relatively irradiation-resistant. It was also demonstrated that only viable normal bone marrow cells are capable of transferring antibody-forming capacity to irradiated recipient rabbits. Neither sonicates nor heat-killed preparations of normal rabbit bone marrow cells possessed this capacity.

Animals↗
PubMed1974

Effect of Lh-Rh on antibody formation, sperm count and plasma levels of gonadotropins and testosterone in normal men.

Synthetic LH-RH was given to 15 healthy men divided into 3 groups of 5 each. A dose of 250 mug LH-RH was injected as a single intravenous bolus for 1 day, every other day for 3 days or for 7 consecutive days respectively. Antibody formation against this synthetic hormone was measured by testing for binding with 125I labeled LH-RH. No antibody formation was detected in any group during the seven day period. Sperm counts were done 1 week before and immediately after the administration of LH-RH, as well as 3 months later. Changes in sperm counts could not be related to the number of injections received. Gonadotropins (FSH and LH) were measured by RIA. There was a significant rise in plasma levels of both gonadotropins, but no signigicant changes in their basal level or percent response resulted from the repetitive administration of LH-RH. Plasma testosterone was also measured by RIA. There was no significant channge in either baseline or percent response in any of the groups after 1, 3 or 7 injections. Some individuals did show a significant rise in plasma testosterone levels, but this was not consistent and was not related to the number of injections administered. Thus, in this study, the repetitive administration of LH-RH did not alter pituitary responsiveness or result in antibody formation.

Adolescent↗
PubMed2004

Clinical impact of antibody formation to botulinum toxin A in children.

We studied the clinical impact of neutralizing antibodies to botulinum toxin A that occurred during long-term treatment of children between 1993 and 2001. Antibodies were found in high titers in 35 of 110 (31.8%) samples from individual patients. Antibody formation correlated with secondary nonresponse (p < 0.001). The most significant risk factors for antibody formation were the frequency of treatments (p = 0.0001) and the injection of a higher weight-adapted maximum dose per treatment (p = 0.001).

Adolescent↗