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At least 667 records · Page 37Linked to original sources
PubMed1999

Development of T-cell memory against inhalant allergens: risks for the future.

Recent evidence suggests that the development of chronic allergic respiratory disease is a biphasic process. Phase 1 commonly occurs during early childhood and in many instances appears to be initiated in utero. This involves initial priming of the Th-cell system against ubiquitous environmental allergens, and subsequent reshaping of these responses during infancy into Th1- or Th2-polarized immunological memory. The second phase of the process comprises the repeated expression of Th2-polarized allergen-specific immunity at the level of the airway mucosa, producing cumulative damage to local tissue resulting ultimately in phenotypic changes including development of airways hyperreactivity. It is also clear that this second phase occurs in only a relatively small subset of subjects who develop long-term Th2-polarized allergen-specific immunity, given that the majority of skin prick test positive subjects do not develop chronic airways disease. This suggests that an additional set of control mechanisms, which regulate the intensity/duration of local Th-cell responses within airway mucosal tissues, may play an important role in the ultimate expression of chronic immunoinflammatory disease in the airways in 'at risk' atopic subjects.

Air Pollutants↗
PubMed2001

Protection of mice with a tuberculosis subunit vaccine based on a fusion protein of antigen 85b and esat-6.

In this study, we investigated the potential of a tuberculosis subunit vaccine based on fusion proteins of the immunodominant antigens ESAT-6 and antigen 85B. When the fusion proteins were administered to mice in the adjuvant combination dimethyl dioctadecylammonium bromide-monophosphoryl lipid A, a strong dose-dependent immune response was induced to both single components as well as to the fusion proteins. The immune response induced was accompanied by high levels of protective immunity and reached the level of Mycobacterium bovis BCG-induced protection over a broad dose range. The vaccine induced efficient immunological memory, which remained stable 30 weeks postvaccination.

Animals↗
PubMed1990

Simian immunodeficiency virus is restricted to a subset of blood CD4+ lymphocytes that includes memory cells.

HIV and the related simian immunodeficiency virus (SIV), which causes AIDS in macaques, infect only a small percentage of CD4+ lymphocytes at any point during the disease. We have identified three distinct cellular phenotypes within the CD4+ subpopulation in macaques, based on cell surface expression of CD44 and CD45R, which putatively represent successive stages of postthymic proliferation and functional maturation. Two of these subsets, CD44hi CD45R+, which contained virtually all circulating cells in cycle, and CD44hi CD45R-, which was noncycling and has been linked to immunologic memory, were selectively depleted in SIV-infected animals at an asymptomatic stage of disease. To test whether SIV infection was restricted to cells with this phenotype in vivo, we used the polymerase chain reaction to sensitively detect SIV DNA in purified subpopulations of CD4+ lymphocytes. We found that SIV exclusively infected blood lymphocytes expressing high levels of CD44. Within this subset infection occurred not only in the fraction containing actively proliferating cells (CD45R+), but also in resting, putative memory cells (CD45R-). These data directly demonstrate that cellular maturation stages of normal postthymic T lymphocyte differentiation are important factors in permitting lentivirus infection in vivo, and that noncycling, memory T cells may be a reservoir for SIV.

Animals↗
PubMed2001

Antigen presentation using novel particulate organelles from halophilic archaea.

A presentation vehicle was developed based on particulate gas vesicles produced by halophilic archaea. Gas vesicle epitope displays were prepared using standard coupling methods or recombinant DNA technology. When presented in the context of gas vesicle preparations, either the hapten, TNP, or a model six amino acid recombinant insert in the outer gas vesicle protein, GvpC was rendered immunogenic. Assays to quantify humoral responses indicated that each preparation elicited strong antibody responses in the absence of exogenous adjuvant. Thus, each preparation elicited a humoral response when injected into mice and this response was long lived and exhibited immunologic memory. Recombinant gas vesicle preparations therefore constitute a new, self-adjuvanting carrier/display vehicle for presentation of an array of peptidyl epitopes.

Adjuvants, Immunologic↗
PubMed2001

Immune checkpoints in viral latency.

The dynamics of the relationship between the immune system and latent viruses are highly complex. Latent viruses not only avoid elimination by the host's primary immune response, they also remain with the host for life in the presence of strong acquired immunity, often exhibiting periodic reactivation and recurrence from the latent state. The continual battle between reemergent infectious virus and immunological memory cells provides an essential virus-host regulatory loop in latency. In this review, we speculate on the critical importance of immune interference mechanisms by viruses contributing to the regulatory loop in viral homeostasis of latency. Central to the notion of viral homeostasis, we further invoke the concept of threshold limits in naive and memory states of immunity to account for the failure of the host to completely eradicate these intracellular parasites.

HIV↗
PubMed2003

Development and regulation of cell-mediated immunity in experimental leishmaniasis.

The development of a Th1 response is critical for controlling many intracellular pathogens. Our laboratory has focused on the role IL-12 plays in initiating such a Th1 response following infection with the obligate intracellular protozoan, Leishmania. Infection of several mouse strains with L. major is associated with IL-12 production and the development of a Th1 response and resistance, although, interestingly, some species of Leishmania (L. mexicana and L. amazonenesis) fail to initiate a Th1 response in the same mouse strains. Consistent with these observations was our finding that IL-12 is an effective adjuvant for the induction of a Th1 response in leishmaniasis (1). Surprisingly, however, in spite of the fact that following resolution of a primary leishmanial infection there is substantial and long-lived resistance to reinfection, an effective prophylactic or therapeutic vaccine for human leishmaniasis does not exist. Our ability to induce a Th1 response in a primate Leishmania vaccine model, but not protection, suggests that long-term resistance to Leishmania requires more than simply initiating a Th1 response (2). Therefore, we recently expanded our studies to investigate how infection-induced resistance to Leishmania operates. We made the unexpected finding that IL-12 is required for L. major-infected mice to remain immune (3). We are now studying how IL-12 participates in maintaining cell-mediated immunity, and more broadly, how immunologic memory works in L. major-healed mice, as well as defining parasite factors that may block the development of cell-mediated immunity.

Animals↗
PubMed1998

Interleukin-10 abrogates the inhibition of Epstein-Barr virus-induced B-cell transformation by memory T-cell responses.

In vitro infection of human B lymphocytes by Epstein-Barr virus (EBV) results in their growth transformation and establishment of immortalized lymphoblastoid cell lines. The virus was found to encode a homologue of the pleiotropic cytokine interleukin-10 (IL-10), which has wide-ranging effects on the immune system. We investigated the effect of human IL-10 (hIL-10) and viral IL-10 (vIL-10) on EBV-specific immunological memory, as assessed by the inhibition of EBV-induced B-cell transformation by the autologous T cells. We found that IL-10 abrogates the inhibitory capacity of T cells. This IL-10 effect is mediated through suppression of T-cell activation-induced IL-2 and interferon-gamma production and through a direct enhancement of EBV-infected B-cell growth.

B-Lymphocytes↗
PubMed1986

Induction of TNP-specific cytotoxic T lymphocyte memory in vivo in the absence of T helper cell activity.

The question of whether TH cells are required for the priming of CTL precursors (CTLp) in vivo was studied by using Txbm mice (Thymectomized, irradiated, and stem cell-reconstituted mice). In these mice, TNP-specific CTL could be induced in vitro with TNP-coupled spleen cells only if the cultures were supplemented with an IL 2-containing supernatant (ConAsup). In contrast to normal mice, TNP-specific Lyt-2-TH cells could not be induced by skin painting with trinitrochlorobenzene (TNCB) (as tested by the ability to help CTL formation from thymocyte or normal spleen precursors). These data confirm previous findings that Txbm mice possess CTLp but that their TH compartment is deficient. TNCB skin painting had, however, a clear priming effect on the CTLp population: spleen cells from TNCB-painted mice could give rise to specific CTL with a lower amount of ConAsup than spleen cells from unprimed mice. In addition to this, priming changed the CTLp so that stimulation with lightly coupled cells (0.1 mM trinitrobenzene sulfonic acid [TNBS] instead of 10 mM TNBS) became effective. These changes took place without a significant increase in the frequency of TNP-specific CTL precursors. The data obtained are consistent with the concept that at least with some antigens, CTLp proliferation (clonal expansion), which is probably caused by activated TH cells, is not required for the induction of immunologic memory in vivo.

Animals↗
PubMed2006

Immunogenicity of cytopathic and noncytopathic viral vectors.

The impact of cytolytic versus noncytolytic viral infections on host responses is not well understood, due to limitations of the systems that have been used to address this issue. Using paired cytopathic and noncytopathic rabies viruses that differ by only two amino acids, we investigated several fundamental aspects of the immune response to these viral vectors. Greater cytopathic capacity translated into a greater degree of cross-priming to CD8(+) T cells (T(CD8)(+)) and more-robust short-term humoral and cellular responses. However, long-term responses to the two viruses were similar, suggesting that direct priming drives the bulk of the T(CD8)(+) antirabies response and that enhanced acute responses associated with greater virally mediated cellular destruction were balanced by other factors, such as prolonged antigen expression associated with noncytopathic virus. Such compensatory mechanisms may be in place to ensure comparable immunologic memories to various pathogens.

Animals↗
PubMed2003

Vaccination strategies. An overview.

Existing vaccines have contributed significantly to the reduction of the mortality and morbidity burdens of many infectious diseases. In many instances, however, the development of these vaccines has been empirical. Furthermore, the impressive progress in the field of vaccines has been mainly driven the progress in molecular biology and microbiology more than by the progress in immunobiology. Nevertheless, the new challenges vaccinology is facing nowadays can be approached through a comprehensive understanding of the mechanisms behind the induction and the maintenance of efficacious immune responses triggered by vaccines. The new vaccination strategies aim at exploiting the new knowledge in the field of dendritic cells (DC; and their role in priming immune responses), in the field of antigen processing and presentation for the generation of antigen-specific cytolytic T cells, and in the field of induction and maintenance of immunological memory, with the ultimate goal of developing better vaccines with an enhanced safety and efficacy not only in children and adults, but also at neonatal age.

Animals↗
PubMed1962

Autoradiographic studies on the immune response.I. The kinetics of plasma cell proliferation.

The origin and growth kinetics of plasma cells have been investigated using autoradiographic labeling techniques. Rats immunized once with Salmonella flagella were given a single pulse of H(3)-thymidine 4 or 40 weeks later. 2 hours after the tracer injection, they received a secondary antigenic stimulus. When animals were sacrificed immediately only certain cells from the resting primarily immunized lymph nodes, notably large and medium lymphocytes, were labeled. Subsequent to secondary stimulation, animals were killed at intervals; nearly all the plasma cells formed within the next 5 to 6 days were labeled. They must thus have been the progeny of cells already capable of synthesizing DNA in resting nodes, most probably of large lymphocytes. Plasmacytopoiesis began with little or no lag following secondary immunization, and the number of labeled plasma cells rose exponentially between the 2nd and 4th day, with a doubling time of about 12 hours. Studies of mean grain counts of primitive cells also suggested that the generation time of plasmablasts was 12 hours or less. The hypothesis was proposed that immunological memory depended on the persistence, following primary stimulation, of a continuously dividing stem line of primitive lymphocytes, reactive at all times to further antigenic stimulation.

Animals↗
PubMed1976

Studies on the immune response to fixed antigens. Preferential induction of helper function with heavily trinitrophenylated sheep erythrocytes, and glutaraldehyde-treated sheep erythrocytes.

Mice primed with heavily trinitrophenylated sheep red cells (TNP128SRC) or glutaraldehyde-treated sheep red cells (G-SRC) developed an early helper function mediated by thymus-derived cells. Such mice were able to produce high secondary responses to both hapten and carrier after challenge 2 days after priming, with lightly trinitrophenylated SRC (TNP0.14SRC). However, the primary response of the TNP128SRC or G-SRC-primed mice were very low to undetectable, and their secondary responses were also low when the challenge antigen was administered 4 days after priming or later. Inhibitory humoral factor(s) which were induced in the primed animals appeared responsible for the decreased capacity of primed mice to mount a secondary response when challenged later than 2 days after priming. Transfer of spleen cells from TNP128SRC-primed mice to sublethally irradiated recipients circumvents their exposure to inhibitory humoral factor(s) present in intact animals allowing them to react with challenge antigen. Enriched populations of T cells, but not B cells, were able to transfer this early immunologic memory to irradiated recipients. The theoretical and practical implications of these results are discussed.

Aldehydes↗
PubMed1995

Submitogenic concentrations of anti-CD3 monoclonal antibody exert antiapoptotic effects in preactivated CD4+ but not CD8+ human T cells.

Immunological memory has been ascribed to the presence of long-lived memory cells. The mechanisms underlying their generation are not completely understood, but dependence on antigen persistence has been discussed in this regard. However, in spite of in vivo evidence favoring this model, studies on TCR/CD3 stimulation of T cell lines or unseparated peripheral blood T cell in vitro have failed to demonstrate prolonged survival of preactivated cells. We have examined the dose-dependent effect of TCR/CD3 engagement mimicked by immobilized anti-CD3 antibody. To this end, well-defined populations of CD4+ and CD8+ lymphoblasts isolated from bulk cultures of preactivated PBMCs by flow sorting were examined. These cells were restimulated with immobilized anti-CD3 in the presence or absence of various costimulatory factors, and were analyzed for their viability state, as well as their apoptotic and proliferative behavior. We have shown that inhibition of apoptosis following CD3 stimulation occurs at submitogenic concentrations, while activation-driven apoptosis requires high-density TCR/CD3 activation. Prevention of apoptosis by submitogenic CD3 stimulation was, however, observed only when CD4+ but not when CD8+ cells were investigated, and was not readily influenced by other costimulatory factors present in cultures. This observation points to the importance of antigen persistence in regulating survival of memory CD4+ but not CD8+ cells.

Antibodies, Monoclonal↗
PubMed1991

Proliferation of lymphocyte-like cells from the solitary tunicate, Styela clava, in response to allogeneic stimuli.

Lymphocyte-like hemocytes (LLCs) of solitary tunicates proliferate in response to allogeneic stimuli. In vitro labeling of proliferative hemocytes from the solitary species Styela clava revealed significantly greater proliferative activity among individuals immunized with allogeneic tissue as opposed to autogeneically primed and naïve animals. Enhanced proliferation was restricted to discrete crypts of dividing cells within the body wall of recipients. Here, increased proliferative activity was specifically associated with LLCs. These data support previous results which implicated LLC activity with immunological memory that is evident in allograft rejection. Hence, it is postulated that adaptive histoincompatibility responses in solitary tunicates depend upon the specific proliferation of immunocompetent cells.

Animals↗
PubMed1976

RES blockade: effects on immunity and tolerance.

Reticuloendothelial cell blockade has been studied for decades in regards to physiological and immunological effects. "Overloading" of RE cells with inert colloidal particles, such as carbon or other particulate substances, has often been used to analyze the role of phagocytic activities in antibody formation, often with contrasting results. In the present studies the effects of colloidal carbon treatment of mice on immunologic responsiveness to sheep erythrocytes was investigated. Pre-treatment of mice with carbon shortly before either primary or secondary immunization with SRBCs markedly suppressed the expected antibody response, as shown by depressed numbers of hemolytic antibody plaque forming cells. Carbon treatment did not affect antibody forming cells per se as shown by lack of an effect on plaque forming cells when carbon was given after SRBCs, either in vivo or in vitro. Carbon injection before primary immunization prevented development of "immunologic memory," as shown by an altered secondary immune response. Mice given carbon and SRBC several weeks before secondary immunization with RBCs developed a primary type antibody response characterized by appearance of 19S antibody with little or no 7S hemolysins, characteristic of a secondary response. Furthermore, by appropriate treatment of mice with carbon and SRBC, immunologic unresponsiveness to SRBCs could also be induced, as evident by absence of both 19S and 7S antibody formation after subsequent challenge immunization with sheep erythrocytes. The mechanisms involved in RE "blockade" induced aberrations of normal immune responses may be related to effects on macrophages or soluble humoral factors, or both. It is unlikely that carbon treatment affects immunocytes directly. Further studies concerning the nature and mechanism of RE blockade on cellular and humoral components of the immune response mechanisms seem warranted and should provide more insight concerning the role of macrophages in antibody formation.

Animals↗
PubMed2003

Significant variation in serotype-specific immunogenicity of the seven-valent Streptococcus pneumoniae capsular polysaccharide-CRM197 conjugate vaccine occurs despite vigorous T cell help induced by the carrier protein.

Streptococcus pneumoniae capsular polysaccharides (PnPSs) induce protective antibodies but are T cell-independent type 2 antigens and are poorly immunogenic in infants. Conjugate vaccines of PnPSs linked to proteins like cross-reactive material (CRM(197)) increase PS antibody titer and elicit immunologic memory in infants. Despite being linked to an identical carrier protein, each PS component of the 7-valent PnPS-CRM(197) vaccine has different immunogenicity. To determine whether variations in conjugate-induced memory T cell responses or PnPS-specific antibody-secreting cells (ASCs) were responsible for serotype-specific differences in immunogenicity, adults were immunized with 7-valent PnPS-CRM(197), and antibody titer, vaccine component-specific CD4(+) T cell recall response, numbers of PnPS-specific ASCs, and cytokine production were measured. PnPS-CRM(197) induced significantly different serotype-specific antibody titers, despite vigorous T cell recall responses to all 7 vaccine components, and production of interleukin (IL)-2, IL-5, IL-6, IL-10, and interferon-gamma. We conclude that PnPS-CRM(197) induces variable serotype-specific antibody titers, despite induction of comparable CRM(197)-specific memory T cell responses.

Adult↗
PubMed1985

Immunity and protection of mice against Neisseria meningitidis group B by vaccination, using polysaccharide complexed with outer membrane proteins: a comparison with purified B polysaccharide.

A methodology for preparing outer membrane proteins (type specific) complexed to group B polysaccharide of Neisseria meningitidis is described. These complexes, low in nucleic acid and lipopolysaccharide content, were immunogenic in mice with induction of humoral antigroup B and antiprotein responses. Immunized mice were also protected against challenge with N. meningitidis group B strains of the same or a different type from that used for vaccination. Both immunity and protection were enhanced when the mice received a secondary immunization with the protein-polysaccharide complex. Additional data have shown the capacity of purified B polysaccharide to induce immunological memory, even though it is incapable of inducing a humoral response when given alone.

Animals↗
PubMed2005

Th2-associated local reactions to the acellular diphtheria-tetanus-pertussis vaccine in 4- to 6-year-old children.

Acellular vaccines against diphtheria-tetanus-pertussis (acellular pertussis) (DTaP) are being progressively introduced into vaccination programs worldwide, with the aim of reducing T-helper 1 (Th1)-associated reactogenicity associated with the cellular diphtheria-tetanus-pertussis (whole-cell pertussis) (DTwP) vaccine. The DTaP vaccine has an improved safety profile in infants, but little information is available concerning the nature of the ensuing immunological memory in older children and how this may affect the reactogenicity of DTaP booster doses. We have addressed this question in the present study by assessing polyclonal and vaccine antigen-specific humoral and cellular immune responses to boosting with DTaP in 4- to 6-year-old children primed during infancy with DTaP (n = 30) or DTwP (n = 16) and by correlating these parameters, in particular cytokine responses, with expression of local side effects at the injection site. Large local reactions (> or =50-mm diameter) 24 to 72 h after receiving the DTaP booster occurred in 43% of exclusively DTaP-primed children, in contrast to 6% of children primed with DTwP. These reactions were associated with vigorous T helper 2 (Th2)-polarized memory responses to vaccine antigen exemplified by interleukin 5 (IL-5), IL-6, and IL-13 production and log-scale boosting of tetanus-specific immunoglobulin E and occurred most frequently among children who are intrinsically "high Th2 responders" as detected by in vitro responsiveness to polyclonal mitogen. Our findings suggest that priming during infancy with DTaP promotes stable, boostable Th2-polarized immunity against vaccine antigens, which in a significant subset of children is subsequently associated with local reactions at the booster site. The time course of these reactions suggests that the underlying mechanism involves reactivation of Th2-polarized cellular immune memory.

Antibody Formation↗