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PubMed1976

[Stimulation of secondary immune response to antigen D from the Rh system].

The authors report the results of investigations on stimulation of secondary immunological response in 30 subjects immunized with antigen D for obtaining highly active sera for production of anti-D immunoglobulin. The analysis of these results showed that application of frequent antigenic stimuli leads to a short-term rise in the antibody level but in 10 cases no expected effect was obtained. None of the immunized subjects produced serologically detectable antibodies reacting with platelets.

Blood Platelets↗
PubMed1989

In vivo modulation of CD1 and MHC class II expression by sheep afferent lymph dendritic cells. Comparison of primary and secondary immune responses.

The experiments described in this article characterize the phenotypic and functional changes in afferent lymph cell populations that occur as a result of in vivo immune stimulation. During the primary immune response (in antigen-naive sheep) there are very transient increases in level of CD1 expression by subpopulations of dendritic cells (DC) but no alterations in cell kinetics or MHC class II expression. In contrast, secondary antigenic challenge (in primed sheep) into the drainage area of an afferent lymphatic causes profound changes in the cell output, characterized by a greater than threefold drop in total cell output on days 1-3 followed by an approximate fivefold rise on day 5. There is also a substantial increase in both the proportion of MHC class II-positive T lymphocytes (from 28 to 54%) and in the quantitative expression of class II by both DC and lymphocytes. Class II expression by DC increases five- to sixfold by day 5, while the level of expression of class II on lymphocytes approximately doubles. The increase in CD1 expression during the secondary response is more prolonged than during the primary response, being detectable between days 2 and 6 after challenge. The rise in class II affects the whole DC population, in contrast to CD1 where the increase affects only a subpopulation of cells. In terms of functional properties, afferent lymph DC isolated during a primary response show no alteration of their activity, whereas DC taken 4-5 d after secondary challenge are up to fivefold more active in their ability to present soluble antigen to primed autologous T cells and to antigen-specific cell lines as well as to stimulate in the MLR. The relative expression of class II correlates temporally with an increased capacity of DC to present antigen. Monoclonal anti-class II antibodies totally inhibit the in vitro assays but anti-CD1 antibodies have no effect. The previous paper has demonstrated that afferent DC can associate with antigen in vivo and can present that antigen to antigen-specific T cells. This article extends our knowledge of DC biology and demonstrates that DC, activated during secondary in vivo immune responses, have an enhanced ability to present an antigen, unrelated to that used for challenge, to specific T cell lines. This enhancement correlates directly with quantitative variation of expressed class II and not CD1 and suggests that this variation in class II expression plays a physiological role in in vivo immune regulation.

Animals↗
PubMedDate not supplied

The ultrastructure of the abdominal lymph nodes cortex in rats during primary and secondary immune response (a special reference to dendritic reticulum cells and interdigitating cells).

The stimulation of coeliac rat lymph nodes was performed by intraperitoneal injections of typhoid vaccine and was unique for the primary immune response and repeated after 6 weeks for the secondary response. The light and electron microscopic observations showed for the primary response, an early germinal center reaction, which might be accounted for by a background of continuous stimulation of the coeliac nodes, stemming from the digestive tract. The dendritic reticulum cells (DRC), considered typical for the B area, were located at the borderline between the germinal center and the mantle zone. Their cytoplasmic extensions penetrated the lymphocyte-lymphoblastic center, surrounding most of the germinal center cells. The marginal zone and the paracortex reacted as a whole, the interdigitating cells (IDC) being the dominant feature. An explanation would be that the marginal zone can be penetrated by T cells and connected IDCs, thus, the B and T areas seem to be largely interspersed. The results suggest that IDCs are cells of direct monocytic origin.

Abdomen↗
PubMed1984

[Terminal B-cell maturation and immunoglobulin synthesis in vitro in primary and secondary immune deficiencies].

Peripheral blood lymphocytes (PBL) from patients with various forms of primary and secondary immunodeficiencies and from 30 healthy control persons were examined for their capacity to show terminal B-cell maturation and immunoglobulin (Ig) synthesis in vitro following pokeweed mitogen (PWM) stimulation. PBL were cultured for 9 days with or without PWM and the percentages of B-cells or plasma cells with strongly positive cytoplasmic Ig (CIg+) were determined by indirect immunofluorescence on methanol fixed cytocentrifuged lymphocyte smears. In addition, newly synthesized IgA, IgG and IgM was measured in the cell free culture supernatant by means of a sensitive microplate ELISA. In 29 out of 30 control cultures the proportion of CIg+-cells increased markedly following 9-day stimulation with PWM. CIg+-cells and newly synthesized Ig were significantly correlated. In a group of 18 patients with common variable immunodeficiency (CVID) maturation to CIg+-cells was greatly impaired and the in vitro production of IgA and IgG was reduced. Two infants with severe combined immunodeficiency (SCID) failed to produce Ig prior to and following haplo-identical bone marrow transplantation despite the presence of immature B-cells. A heterogeneous group of secondary immunodeficiencies showed different forms of an impaired terminal B-cell maturation and a reduced capacity to synthesize Ig in vitro. The described PWM culture techniques in combination with the evaluation of CIg+-cells and the measurement of newly synthesized Ig in the culture supernatant proved to be a reliable in vitro correlate for terminal B-cell maturation and represent an important tool for the classification of humoral immunodeficiencies.

Adolescent↗
PubMed1987

[Characterization of secondary immune deficiency in patients with chronic glomerulonephritis].

A study was made of the nature of secondary immuno-deficiency, peculiarities of disordered function of regulatory T-lymphocytes (helpers and suppressors), and their interrelationships in different clinical variants of chronic glomerulonephritis (CGN). Altogether 94 CGN patients were examined, of them 34 were with urinary syndrome and 60 with nephrotic syndrome. With relation to a clinical variant of disease the absolute amount of T-lymphocytes was significantly lowered, the amount and function of B-lymphocytes showed a tendency to an increase. Function of nonspecific Concanavalin A-induced T-suppressors using PHA as a mitogenic indicator (T-T-suppression) was insignificantly raised, and when lipopolysaccharide (T-B-suppression) was used it was considerably suppressed. T-lymphocyte helper activity in CGN patients was on an increase.

B-Lymphocytes↗
PubMed1979

Difference in capacity of Sendai virus envelope components to induce cytotoxic T lymphocytes in primary and secondary immune responses.

Studies were made on the abilities of Sendai virus envelope components to induce primary and secondary generations of virus-specific cytotoxic mouse T lymphocytes (CTL). The primary CTL response in BALB/c mice was induced by reassembled envelope particles that had fusion activity but not by envelope glycoproteins without fusion activity, although both preparations induced a humoral immune response. Reconstitution of membrane-bound envelope proteins from envelope glycoproteins with lipids restored the fusion activity and the capacity to induce CTL. Target cells susceptible to virus-specific CTL could be induced by reassembled envelope particles, but not by envelope glycoproteins or LLC-MK2 cell-grown Sendai virus, neither of which had fusion activity. On the other hand, all the viruses and envelope components tested were found to stimulate a virus-specific CTL response in the in vitro secondary generation of CTL from virus-primed spleen cells. These results suggest that Senaei virus fusion activity is involved in primary induction of the CTL response as well as in target cell formation, but that it is not essential for secondary stimulation of the CTL response.

Animals↗
PubMed1988

A subpopulation of germinal center B cells differentiate directly into antibody forming cells upon secondary immunization.

In the present study we sought to test the hypothesis that GC B cells may be stimulated to differentiate into AFCs during the induction of the secondary antibody response. To test this we gave HRP immune mice a booster immunization and looked for AFCs in the GCs making anti-HRP specific antibody. Within 3 days cells in the GCs were making anti-HRP. Most of the cells were just starting to make immunoglobulin in the rough endoplasmic reticulum but some were nearly mature plasma cells like those in the medullary cords. Furthermore, we isolated GC B cells after a boost with OVA and tested their ability to differentiate directly into AFCs. Data obtained using an OVA specific RIA indicated that purified GC B cells would differentiate and produce specific antibody in the absence of added T cells or antigen. Examination of the cells after 5 days in culture indicated that many of them had differentiated into large plasma cells. These results obtained both in vivo and in vitro demonstrate that shortly after booster immunization GC B cells receive the appropriate antigen and T cell signals in vivo to differentiate and become AFCs.

Animals↗
PubMed1991

[Mechanisms of development of endolymphatic hydrops following secondary immune response in the endolymphatic sac of guinea pigs].

Previously the author reported the immediate development of endolymphatic hydrops (e. hydrops) following direct challenge of secondary antigen to the endolymphatic sac (ES) in guinea pigs, during the early phases of postchallenge, ranging from 1 to 5 weeks. The present study reports the results of specimens taken up to 10 weeks postchallenge, and correlation of e.hydrops to perilymph in antigen-specific antibody levels. From the present results, mechanisms of e.hydrops induced ES immune reaction are suggested as follows. 1) In the early stage of e.hydrops, an acute inflammatory reaction in the ES may produce endolymph by an increased vascular permeability of the inner ear and may impair endolymph absorption from the ES. 2) In the latter stage of e.hydrops, the moderate cellular infiltration in the ES may cause chronic impairment of endolymph absorption in the ES.

Animals↗
PubMed1984

Interference in the development of a secondary immune response in mice by zinc deprivation: persistence of effects.

The purpose of this study was to determine the effects of a moderate period of zinc deficiency on the secondary responses of mice primed with antigen prior to nutritional insufficiency. Adult A/J mice were primed with sheep red blood cells (SRBC) 2 weeks prior to being placed on zinc-deficient, zinc-adequate or intake-restricted diets. After 28 days some of the mice in each treatment group were given a second injection of SRBC. Deficient mice could produce only 43% as many IgG anti-SRBC plaque-forming cells (PFC) per spleen as could the zinc-adequate or restricted-fed mice. To compare the secondary response of cells from each dietary group in a uniform environment, additional mice were killed as a source of primed splenocyte for transfer to irradiated hosts. Compared to controls, splenocytes from deficient mice gave suboptimal secondary responses even in normal irradiated hosts. Finally, the remaining mice were provided with zinc-adequate diet for a period of 4 weeks to allow for repair of the memory response, but it was only partially restored by this means. The data suggest that zinc deficiency may have destroyed a substantial portion of SRBC memory cells.

Animals↗
PubMed1996

Primary and secondary immune responses to Listeria monocytogenes.

Recent studies have revealed the complexity of cytokine and cellular interactions required for resistance to primary Listeria monocytogenes infection and have illustrated that resistance to secondary infection may occur through multiple pathways. Analyses of Listeria epitope generation and the specificity of protective CD8(+) T cells have suggested that future research should focus on secreted protein antigens in specific resistance to infection and have increased our understanding of Listeria antigens presented by MHC class l-b molecules.

Animals↗
PubMed2002

Role of IL-5 during primary and secondary immune response to acetylcholine receptor.

To analyze the role of the Th2 cytokine interleukin-5 (IL-5) in experimental autoimmune myasthenia gravis (EAMG) pathogenesis, we induced clinical EAMG in C57BL/6 and IL-5 gene-knockout (KO) mice in the C57BL/6 background. IL-5 KO mice had a significantly reduced incidence and severity of EAMG. Despite their increased resistance to EAMG, IL-5 KO mice displayed intact secondary antibody and lymphoproliferative responses to acetylcholine receptor (AChR) after immunization with this molecule. However, the relative resistance of IL-5 KO mice was associated with a reduced primary lymphocyte response to AChR, and reduced C3 levels in muscle extracts compared to those in C57BL/6 mice.

Adjuvants, Immunologic↗
PubMed1978

Cell-mediated cytotoxicity: comparison of primary and secondary immune reactions after parainfluenza type 1 virus inoculation.

H-2 antigen compatibility of effector spleen cells and target cells was necessary for cell-mediated cytotoxicity (CMC) after both 1 and 2 intraperitoneal inoculation of 6/94 virus into mice. T cells were responsible for both primary and secondary CMS reactions. Neither reaction was influenced by the presence of virus-specific antibody added to the test system. Secondary CMC peaked earlier than the primary response and declined more rapidly. In vitro stimulation of primed spleen cells could also be used to detect the secondary CMC response.

Animals↗
PubMed1992

Testosterone inhibits the immunostimulant effect of thymosin fraction 5 on secondary immune response in mice.

The purpose of the present investigation was to examine the in vivo influence of testosterone on the immune properties of a thymic factor (thymosin fraction 5, TF5) a partially purified thymic preparation in male Swiss IOPS/OF1 mice (5-10 weeks old). Testosterone administration (100 micrograms/ml) significantly inhibited the enhanced anti-sheep red blood cell antibody response induced by TF5 (100 micrograms/ml); this inhibition was only observed on the secondary antibody response and not on the primary. These results suggest that gonadal steroids can affect the immune response by modulating the activity of thymic factors.

Animals↗
PubMed1979

Immunosupression of the primary and secondary immune response by an IgM plasmacytoma (TEPC-183).

Previously we had established that TEPC-183 IgM(K) suppressed the primary immune response (IR) to both the T-dependent antigens 2,4-dinitrophenyl-haemocyanin (DNP-HCY) and T-independent pneumococcal polysaccharides. In the current investigation, the effect of TEPC-183 on an ongoing immune response to SS-III and DNP-HCY was examined. It was found that when TEPC-183 was injected 6 days after the initial antigen injection, at the height of the primary IR, the response was significantly suppressed to SS-III and to the DNP ligand. In addition, suppression of the secondary IR occurred when mice were injected with tumour as late as 35 days after the first antigen injection. Tumour removal lifted the immunosuppression to DNP and the tumour-removed group had a similar number of both direct and indirect anti-DNP-PFC, although HA levels were still reduced. When mice were pretreated with serum from normal mice or serum or ascites from TEPC-183 bearing mice, one day prior to and on the day of antigen injection, the immune response to DNP was reduced by TEPC-183 serum but not by normal mouse serum (NMS), while the anti-SSS-III response was reduced by both NMS and TEPC-183 serum. Thus, NMS selectively suppressed the T-independent response, but only TEPC-183 serum suppressed both types of responses. The suppressive effect of serum on the IR of normal mice indicates a role for soluble regulatory suppressive factors present in the serum of normal and tumour-bearing mice. The data are consistent with the idea that the tumour exerts its effect on the inductive as well as the proliferative phase of the immune response.

Animals↗
PubMed1989

The MRC OX-22- CD4+ T cells that help B cells in secondary immune responses derive from naive precursors with the MRC OX-22+ CD4+ phenotype.

CD4+ T cells in the rat can be divided into two nonoverlapping subsets by their reactivity with the mAb MRC OX-22, which binds some of the high molecular weight forms of the CD45 antigen. The lineage relationship between subsets of CD4+ T cells expression different forms of CD45 has been a controversial issue for some time. Experiments described in this paper address this question using in vivo assays of T cell reactivity. Analysis of primary antibody responses in vivo show that it is MRC OX-22+ CD4+ T cells that are active in these assays, whereas antigen-primed T cells that provide helper activity for secondary antibody responses in vivo have the MRC OX-22- CD4+ phenotype. It is demonstrated that these memory T cells derive from MRC OX-22+ CD4+ T cell precursors and not from a putative separate lineage. It is concluded that with respect to the provision of help for B cells, MRC OX-22+ CD4+ T cells are precursors of memory cells with the phenotype MRC OX-22- CD4+.

Animals↗
PubMed2006

Treatment of Brucella-susceptible mice with IL-12 increases primary and secondary immunity.

Brucella spp. cause disease in humans and livestock and are potential biowarfare agents. Defining the protective immune response is necessary to design vaccines. This has largely been done with mice, brucella-susceptible BALB/c and resistant C57BL strains. Since interferon-gamma is key to brucella resistance, contrary to expectations, we found that ex vivo splenocytes from naïve BALB/c mice produced IL-12 and interferon-gamma in cultures with brucellae at levels comparable to those of splenocytes from the more resistant C57BL/10 mice. Moreover, both IL-12 and interferon-gamma were produced in the first week following infection of BALB/c mice. However, by the third week of infection we found decreased IL-12Rbeta2 expression by BABL/c splenocytes, corresponding to their inability to produce interferon-gamma in Brucella recall responses at this time as reported previously. Administering recombinant IL-12 to these mice ameliorated the interferon-gamma hiatus, resulted in a 1000-fold reduction in CFU during primary infection and increased survival following secondary challenge.

Animals↗