[Stimulation of primary and secondary immune responses with yeast NaRNA].
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Adjuvants, Immunologic↗
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[Effect of chorionic gonadotropin on formation of secondary immune response].
Experiments were carried out in vivo and in vitro. Secondary immune response to sheep red cells was assessed on day 5 after repeated immunization by IgM and IgG antibody-producing cells. Chorionic gonadotropin was injected after reimmunization to intact and ovariectomized animals in doses compatible to those in normal pregnancy. In vitro chorionic gonadotropin was added for one h into sensitized splenocyte cultures and then its effects were assessed in syngeneic transfer system by the same parameters. Experiments have demonstrated that in dose 40 MU chorionic gonadotropin cannot influence secondary immune response formation. All hormonal effects are related to 200 MU dose extrapolated from the maximal level of this hormone during pregnancy. In this dose gonadotropin reduced splenocyte counts and inhibited the formation of IgG-antibody-producing cells. Ovarian sex steroids do not mediate chorionic gonadotropin immunomodulating effects. An hour's contact of sensitized splenocytes with the hormone in a high dose resulted in a statistically significant inhibition of the formation of IgM-antibody-producing cells. Hence, if chorionic gonadotropin interacted with immunocompetent cells before their repeated contact with the antigen, IgM-antibody-producing cells suffer, and if this exposure occurs after this contact, IgG-antibody-producing cells decrease in number. The role of chorionic gonadotropin in development of normal pregnancy and that complicated by immunopathologic processes is discussed.
Adjuvants, Immunologic↗
A role for IFN-gamma in primary and secondary immunity generated by NK cell-sensitive tumor-expressing CD80 in vivo.
We have investigated the primary and secondary immunity generated in vivo by a MHC class I-deficient tumor cell line that expressed CD80 (B7-1). CD80 expression enhanced primary NK cell-mediated tumor rejection in vivo and T cell immunity against secondary tumor challenge. CD80 expression enhanced primary NK cell-mediated tumor rejection, and both NK cell perforin and IFN-gamma activity were critical for the rejection of MHC class I-deficient RMA-S-CD80 tumor cells. This primary rejection process stimulated the subsequent development of specific CTL and Th1 responses against Ags expressed by the MHC class I-deficient RMA-S tumor cells. The development of effective secondary T cell immunity could be elicited by irradiated RMA-S-CD80 tumor cells and was dependent upon NK cells and IFN-gamma in the priming response. Our findings demonstrate a key role for IFN-gamma in innate and adaptive immunity triggered by CD80 expression on tumor cells.
Animals↗
Induction of secondary immune response by reactivated Japanese encephalitis virus in latently infected mice.
Development of secondary immune response has been studied following reactivation of latent Japanese encephalitis virus (JEV) infection in mice. The virus could be reactivated in 43% of the latently infected mice at 27 weeks p.i. by treatment with cyclophosphamide. The reactivated virus induced delayed-type hypersensitivity (DTH) and leucocyte migration inhibition (LMI) responses in mice, with peak activity on Day 5 post-reactivation (p.r.). The DTH persisted at low levels for long periods. Humoral immunity measured by haemagglutination-inhibiting antibody showed a four-fold rise in antibody titres. DTH was transferable by immune spleen cells for 5 days p.r. only. It is, therefore, concluded that JEV reactivation generates a quick and short-lived secondary immune response.
Animals↗
Single exposure of mice to Borrelia burgdorferi elicits immunoglobulin G antibodies characteristic of secondary immune response without production of interleukin-4 by immune T cells.
Borrelia burgdorferi antigen can elicit immunoglobulins (Igs) characteristic of the primary and secondary immune responses without the contribution of an interleukin-4-producing helper T-cell population. Single exposure of mice to soluble B. burgdorferi antigen elicited both Th1-type and Th2-type antispirochete antibodies. Production of the Ig classes showed different patterns with increasing time postinjection (IgM levels decreased; IgG1, IgG2a, IgG2b, and IgG3 levels increased; IgE was not detected), and Ig patterns were similar to those produced in infected mice. Upon infectious challenge, immunized mice achieved maximal titers of all antispirochete IgG subclasses more quickly than unimmunized mice did. In contrast to the antibody responses which showed both Th1- and Th2-type patterns, T-cell immune response to either immunization or infection was characterized by interleukin-2 and gamma interferon production; interleukin-4 and interleukin-5 were undetectable. Injection with whole spirochetes induced a pattern of antibodies and cytokine production similar to those obtained by injection with soluble antigen. In addition, mouse strains of different major histocompatibility complex backgrounds produced similar patterns of Ig in response to immunization. None of the various parameters of immunization tested resulted in detectable interleukin-4 production by primary or secondary immune T cells. The production of both IgM and IgG1 at early times following a single exposure to spirochete antigen clearly differs from immune responses to haptens or model protein antigens. Production of similar Ig classes in infected and immune mice implies that antigen-specific antibody is responsible for passive immunizing activity found in immune sera.
Adjuvants, Immunologic↗
Vibriolytic IgG immunocyte response of mice after primary and secondary immunization with cholera somatic antigens.
Antibody plaque-forming cells (FC) to the somatic antigens of Vibrio cholerae were enumerated in the spleen of mice after primary and secondary immunization with a heat-killed vaccine prepared from the vibrios. Immunocytes releasing both high efficiency IgM and low efficiency IgG antibody were readily detected using a direct and facilitated plaque procedure in agar gel. Whereas the peak numbers of IgM-PFC after primary immunization occurred on days 12 to 14, the peak IgG-PFC response developed somewhat later (16-18 days). After a second injection of vaccine larger numbers of both IgM- and IgG-PFE appeared in the mouse spleens, with peak responses for both occurring between days 5 and 8. The largest number of IgG-PFC developed in spleens of mice given a second injection of vaccine 6-8 weeks after primary immunization. The dose of killed vibrios used for priming markedly affected both the magnitude and the class of antibody-forming cells appearing during the secondary response; 1--10 mug vaccine was more effective than higher or lower doses for priming the mice to a heightened secondary response. Furthermore, the antigenic specificity of both the IgM- and IgG-PFC appearing after secondary immunization was directly related to the strain of cholera bacilli used for priming. When mice were immunized with the Ogawa strains of cholera most of the secondary PFC after booster immunization with the serologically distinct Inaba strain was directed towards the common antigen shared by both strains and not to the type specific antigen of the Inaba vibrios. The specificity of the anti-vibrio PFC during both the primary and secondary responses was readily demonstrable by inhibition experiments using sonicated or soluble cholera antigens. Prior incubation of these antigens with test spleen cells in the agar gel effictively inhibited development of the vibriolytic plaques, regardless of antibody class. Similar antigen extracts from toher bacteria had no effect. The immunoglobulin nature of the plaques was also demonstrable by inhibition with low dilutions of rabbit anti-mouse globulin serum incorporated into the agar plates prior to testing; both IgM and IgG plaues were inhibited.
Animals↗
Rheumatoid factors and secondary immune responses in the mouse. I. Frequent occurrence of hybridomas secreting IgM anti-IgG1 autoantibodies after immunization with protein antigens.
The involvement of rheumatoid factor (RF)-secreting cells in normal immune responses was examined by screening hybridomas derived from 129/Sv mice during primary and secondary immune responses against foreign proteins. No RF-secreting cells were detected during primary responses, but up to 10% of the total number of clones obtained during secondary responses produced IgM with anti-IgG activity. Like typical mouse RF, these anti-IgG autoantibodies had a strict isotypic specificity, mostly for IgG1, and a much stronger avidity for immune complexes than for native IgG. The selective activation of IgG1-specific RF during these secondary immune reactions was not due to fortuitous antigenic similarities between mouse IgG1 and the antigens used for immunization, nor did it result from the use of adjuvants for priming, or from contamination of antigen preparations with lipopolysaccharide. It is therefore concluded that, in the 129/Sv mouse, RF production during secondary immune responses is a physiological phenomenon.
Animals↗
Binding of autoreactive mouse anti-type II collagen antibodies derived from the primary and the secondary immune response investigated with the biosensor technique.
The reactivity of autoantibodies to type II collagen, secreted by B cells isolated from the primary and the secondary immune response to rat type II collagen in DBA/1 mice, was investigated using BIAcore 2000 instrumentation. Assays were performed on both collagen and antibody surfaces. These assays demonstrated a 100-fold difference in affinity between primary and secondary immune response antibodies. The difference in affinity was almost entirely due to differences in the dissociation rate constant. Somatic mutations in secondary clones were in one case associated with a 3-4-fold difference in affinity and in another case appeared to be without any effect on the binding activity.
Animals↗
The macrophage response in mice after primary and secondary immunization with sheep red blood cells.
A primary and a secondary immune response to sheep red blood cells (SRBC) was evoked in mice by intraperitoneal injection of the antigen. Macrophage proliferation and migration as well as induction of the lysosomal enzyme acid phosphatase in macrophages were assessed along with lymphocyte proliferation. The proliferative responses were evaluated by 3H-thymidine labelling (autoradiography). The secondary response elicited a faster and stronger lymphocyte proliferation than the primary response. This pattern was not seen to apply to the macrophages where the highest proliferative rate was found in connection with the primary response. The macrophages acquired an increased content of acid phosphatase during both types of responses, but the significantly highest level was reached in the secondary response. Large numbers of monocytes migrated into the peritoneal cavity during the first day after immunization. However, macrophage proliferation took place in resident as well as in immigrant cells.
Acid Phosphatase↗
Rheumatoid factors and secondary immune responses in the mouse. II. Incidence, kinetics and induction mechanisms.
Production of IgM rheumatoid factor (RF) during secondary immune responses was studied in normal mouse strains by measuring RF synthesis in spleen cell cultures. A considerable, although transient, RF response was observed in BALB/c and C57BL/6 mice immunized and i.v. boosted with various protein antigens and with sheep erythrocytes. With most antigens, RF production equalled or exceeded that of antigen-specific IgM, but it peaked and subsided earlier. No RF production was detected when either priming or boosting was omitted. The isotypic specificity of RF depended upon the antigens used for immunization: all proteins tested stimulated the synthesis of RF specific for IgG1, whereas sheep erythrocytes induced both IgG1- and IgG2a-specific RF. Reconstitution experiments of irradiated naïve C57BL/6 mice with various combinations of syngeneic antibody against human transferrin and primed or unprimed spleen cells indicated that important RF responses could be induced only when antigen was injected into mice that had received both antibody and immune spleen cells.
Animals↗
Rabbit antibodies to streptococcal carbohydrates. Influence of primary and secondary immunization and of possible genetic factors on the antibody response.
In a search for possible genetic factors which may influence the immune response to the streptococcal carbohydrates, over 100 rabbits have been immunized with streptococcal vaccines, and representative examples of high and low response pairs mated. The concentration of precipitins to the group-specific carbohydrates has been measured in the antisera following primary intravenous immunization with heat-killed streptococcal vaccines, Group A, Group A-variant, and Group C. For the majority of rabbits, the concentration of precipitins varied between 1 and 10 mg/ml of antiserum; while in the minority, it was between 11 and 32 mg/ml. The offspring of rabbits with high antibody levels had a significantly higher concentration of antibody than was seen in the offspring of rabbits of low response parents. Such data suggest that the magnitude of the immune response to these carbohydrate antigens is under some form of genetic control. Not uncommonly in rabbits with hyper-gamma-globulinemia following primary immunization, the group-specific precipitins are the predominant component of the gamma-globulin. An unusual feature of such components is that they are electrophoretically monodisperse, and possess individual antigenic specificity. In this respect they resemble the myeloma proteins. When a response of this sort is not seen after primary immunization, it may occur after secondary immunization. Therefore, prior exposure to the same or closely related antigen may also have an influence on the occurrence of high concentrations of such uniform antibodies.
Animals↗
[Secondary immune response of mice immunized with a protein-cellulose complex].
It has been previously established that an intravenous injection of a protein antigen solution into mice primed with the same antigen in the form of a protein-cellulose complex induces an intensive antibody production (up to 10,000 antibody-forming cells/10(6) splenocytes and up to 3 mg of antibodies/ml of serum). The present study has shown that secondary immune response can be considerably enhanced if large amounts of the antigen are administered intraperitoneally in a protein-cellulose complex during secondary immunization. In these experiments the mean number of antibody-forming cells was 50.000/10(6) splenocytes and the antibody serum level averaged 10 to 12 mg/ml. The effect persisted for a long time: as late as on day 80 the antibody concentration was 2 mg/ml of serum.
Animals↗
Divergent selection of chickens for antibody response to sheep erythrocytes: kinetics of primary and secondary immunizations.
Chicks from lines selectively bred for either high or low antibody response post-primary immunization (PPI) to sheep erythrocytes (SRBC) and their reciprocal crosses were immunized intravenously with 0.1 ml of 0.25% SRBC antigen in Trials 1 and 3 and with 0.1 ml of 0.025%, 0.25%, or 25% SRBC antigen in Trial 2. All initial immunizations were made at 35 days of age, and 0.1 ml of 0.25% SRBC booster dose was given 24 days later. Results showed that (a) population differences appeared by day 4 PPI and persisted through day 24 PPI, (b) regardless of population, peak titers occurred at about the same time for primary and secondary immunizations, (c) dosage of antigen influenced differences among populations in antibody response to primary immunization, and (d) both selected lines had similar responses in 2-mercaptoethanol-sensitive and 2-mercaptoethanol-resistant antibodies to primary but not secondary immunization.
Animals↗
Ultraviolet a irradiation of C57BL/6 mice suppresses systemic contact hypersensitivity or enhances secondary immunity depending on dose.
Ultraviolet radiation is the most common environmental carcinogen humans are exposed to. It is now known that in order for skin cancers to develop, both genetic damage and immunosuppression is required. Ultraviolet-induced immunosuppression is therefore a key contributor to the development of skin cancer. Little is known about the relative contributions of the different ultraviolet spectra (A and B), however. Therefore detailed ultraviolet dose-response curves for systemic suppression of contact hypersensitivity in two mouse strains were determined to examine the relative contributions of each of these spectral components of sunlight to primary and secondary immunity. Whereas ultraviolet B caused a linear dose-related immunosuppression in both C57BL/6 and Balb/c mice, only C57BL/6 mice were immunosuppressed by medium doses of ultraviolet A. At higher ultraviolet A doses, C57BL/6 mice were protected from immunosuppression, suggesting a genetic predisposition to ultraviolet-A-induced immunomodulation. Surprisingly, we found that, in contrast to primary immunosuppression, low dose ultraviolet A enhanced the secondary immune response, whereas ultraviolet B caused antigen-specific tolerance. When ultraviolet A and ultraviolet B were combined to mimic sunlight (solar-simulated ultraviolet), immunosuppression and tolerance were only observed over a narrow dose range as the memory-enhancing effect of low dose ultraviolet A and the immunoprotective effect of higher dose ultraviolet A prevented the suppressive effects of ultraviolet B. These studies suggest that complex relationships between ultraviolet dose, immunomodulation, spectra, and genetic background are likely to be important for skin cancer induction. We also describe for the first time that low doses of ultraviolet A are able to enhance secondary immunity, which has important implications for vaccination strategies.
Animals↗
Lymphocyte differentiation and antibody synthesis in the secondary immune response of peroxidase stimulated lymph nodes of rat.
Lymphocyte differentiation and specific antibody synthesis were studied in the course of the secondary immune response of horseradish-peroxidase immunized rat popliteal lymph nodes by electron microscopic immunocytochemistry. From primary immunization, mature plasma cells containing specific antibody remained as long as 10 months. Antihorseradish peroxidase antibodies were localized in lymphocytic blast cells on Day 3 after restimulation with antigen. In the subsequent days blast cells were still present, and shifting to mature stages occured. During immunocyte differentiation and maturation vesicles and tubules of the Golgi complex became filled with specific antibody suggesting occasional secretion of antibody via the Golgi apparatus. At very mature cell stages, antibody was accumulated in distended cisternae.
Animals↗
[Characteristics of the immunomorphological substrate in secondary immunization as dependent on the functional state of the hypothalamic nuclei].
The authors traced the morphological and serological shifts occurring in secondary immunological response against the background of destruction of the posterior hypothalamic nuclei. It was revealed in experiments on rabbits that in primary and secondary immunization carried out against the background of bilateral coagulation of the posterior hypothalamic nucleus the secondary immunological response was reduced in comparison with control. Depression occurred both on account of reduction of the number of cells-precursors, and in connection with disturbances of differentiation of the antibody-forming cells. When the primary immunization was conducted against the background of the intact brain, and destruction of the posterior hyfothalamic nuclei preceded the secondary immunization there occurred a change in the number of cells-precursors involved in differentiation, without disturbance of the differentiation itself.
Animals↗
A limited number of B cell lineages generates the heterogeneity of a secondary immune response.
We have studied the cellular basis for heterogeneity in the secondary immune response by creating a large set of B cell hybridomas from a single C57BL/6 mouse immunized with the hapten (4-hydroxy-3-nitrophenyl)acetyl coupled to chicken gamma-globulin, and searching among the cells for all possible sets of clonally related lines. Among 28 independent cell lines from a single animal we find that 21 of them fall into seven small families of from two to five members; only seven lines have no matches among the set. A statistical analysis determines that the number of genetically distinct B cell precursors whose progeny were isolated during this secondary response is 18, with 95% confidence limits of 14 and 26. The distribution of family sizes implies that each activated clone has proliferated to approximately the same extent. Complete sequencing of the variable region of immunoglobulin heavy chain mRNA from 19 of the cell lines reveals many shared somatic mutations among related lines, implying a pronounced founder effect has occurred to eliminate most of the progeny of each precursor B cell. This may be the result either of a high frequency of debilitating somatic mutation or from selection against cells still expressing the idiotype of primary anti-(4-hydroxy-3-nitrophenyl)acetyl antibodies.
Animals↗
[The effect of chorionic gonadotropin on the formation of a secondary immune response].
Investigations have been carried out in experimental systems in vivo on noncastrated and ovariectomized female [correction of male] mice and in vitro. The secondary immune response to sheep erythrocytes has been estimated on the 5-th day after reimmunization by IgM and IgG levels in the antibody-forming cells (AFC). It has been established, that in a dose of 40, IU, chorionic gonadotropin (CG) does not influence the formation of a secondary immune response. All the effects of the hormone are associated with the dose of 200 IU, extrapolated from the maximum CG level during pregnancy. CG in this dose reduces spleen cellularity and suppresses the PFC formation processes. Ovarian sexual steroids do not mediate CG immunodepressive effects, but they are able to abolish the effect of G-AFC depression. An hour preincubation of CG (200 IU) with sensitized splenocytes in vitro suppresses M-AFC formation processes. So, if CG (200 IU) interacts with immunocompetent cells before their repeated contact with antigen, the M-AFC counts decreases; after reimmunization the G-AFC counts decreases.
Adjuvants, Immunologic↗