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At least 469 records · Page 26Linked to original sources
PubMed1987

Long-term cholera antitoxin memory in the gut can be triggered to antibody formation associated with protection within hours of an oral challenge immunization.

A local mucosal immunological memory that could be efficiently triggered to protective antibody formation on renewed antigen exposure might account for the several-year long protection against reinfection and disease seen in individuals after cholera disease. The duration and other functional aspects of gut mucosal immunological memory to the cholera toxin (CT), which is the key pathogenic factor in cholera, were examined in mice. Six months or even 2 years after an initial series of oral immunizations with CT a single repeat oral exposure to CT in submicrogram amounts evoked a brisk IgA antitoxin response in the lamina propria. A three-fold increase in IgA antitoxin-producing cells (SFC) was evident within 16 h, with a further rise in SFC numbers over the next several days. The anamnestic gut mucosal IgA antitoxin response was associated with a substantial increase in protection against challenge of intestinal loops with CT. The rapid increase in IgA antitoxin SFC in the gut is believed to reflect memory cells dispersed in the gut mucosa which can be rapidly triggered into antitoxin formation by antigen encounter in vivo and such cells could clearly be responsible for the long-term immunity seen after cholera disease or oral vaccination.

Animals↗
PubMed2003

IL-15R alpha expression on CD8+ T cells is dispensable for T cell memory.

The generation and maintenance of immunological memory requires the activation, expansion, and persistent proliferation of antigen-specific T cells. Recent work suggests that IL-15 may be important for this process. Surprisingly, we now find that expression of the high-affinity receptor for IL-15, IL-15R alpha, on T cells is dispensable for the generation or maintenance of memory CD8(+) T cells. By contrast, IL-15R alpha expression on cells other than T cells is absolutely critical for this function. These findings may be related to IL-15R alpha's ability to present IL-15 in trans to low-affinity IL-15R beta gamma(c) receptors on memory CD8(+) T cells. These unexpected results provide insights into how IL-15R alpha supports memory CD8(+) T cells.

Adjuvants, Immunologic↗
PubMed1986

Intestinal mucosal memory and presence of memory cells in lamina propria and Peyer's patches in mice 2 years after oral immunization with cholera toxin.

The build-up of long-term immunological memory in the gut mucosal immune system may explain long-lasting protection against new attacks of cholera in convalescents from natural disease. We have looked for gut mucosal antitoxin immunological memory and memory cells in mice after oral immunization with cholera toxin. Our results show that mice that were orally primed with cholera toxin and then boosted 2 years later with a single oral antigen dose mounted a rapid and vigorous IgA antitoxin response in the intestinal lamina propria. A specific secondary antitoxin response could also be elicited without any in-vivo boosting by in-vitro stimulation of isolated lymphocytes from the lamina propria, Peyer's patches, mesenteric lymph nodes, and spleen. The results provide evidence for the almost life-long persistence of anti-cholera toxin memory B cells (and perhaps also T cells) in the intestine and probably also recirculating cells, after oral immunization with cholera toxin. A functional antitoxic immune response may be boosted rapidly on renewed enteral exposure to cholera toxin by the stimulation of memory cells both in the lamina propria and in the Peyer's patches.

Administration, Oral↗
PubMed2001

T-cell immunity in the induction and maintenance of a tumour dormant state.

We conclude from animal tumour model studies that T cell immunity can play an essential role in the induction and maintenance of tumour dormancy. Evidence was found in tumour dormancy situations for active control of proliferating tumour cells by CD8 memory T cells leading to a long-term balance in the bone marrow between low numbers of tumour cells and immunological memory. In breast cancer patients, too, the bone marrow may represent a privileged compartment for tumour dormancy and immunological memory. Upon restimulation with tumour antigen pulsed autologous dendritic cells, bone marrow-derived memory T cells from cancer patients could be shown to exist and to become activated into potent anti-tumour effector cells.

Animals↗
PubMed2004

DNA vaccine encoding human immunodeficiency virus-1 Gag, targeted to the major histocompatibility complex II compartment by lysosomal-associated membrane protein, elicits enhanced long-term memory response.

Antigen presentation by major histocompatibility complex type II (MHC II) molecules and activation of CD4+ helper T cells are critical for the generation of immunological memory. We previously described a DNA vaccine encoding human immunodeficiency virus-1 p55Gag as a chimera with the lysosome-associated membrane protein (LAMP/gag). The LAMP/gag chimera protein traffics to the MHC II compartment of transfected cells and elicits enhanced immune responses as compared to a DNA vaccine encoding native gag not targeted to the MHC II compartment. We have now investigated the long-term responses of immunized mice and show that the LAMP/gag DNA vaccine promotes long-lasting B cell- and CD4+ and CD8+ T-cell memory responses induced by DNA encoding non-targeted Gag decay rapidly and elicit very low or undetectable levels of gag DNA is sufficient to generate T-cell memory. Following this initial priming immunization with LAMP/gag DNA, booster immunizations with native gag DNA or the LAMP/gag chimera are equally efficient in eliciting B- and T-cell secondary responses, results in accordance with observations that secondary expansion of CD8+ cells in the boost phase does not require additional CD4+ help. These findings underscore the significance of targeting DNA-encoded vaccine antigens to the MHC II processing compartments for induction of long-term immunological memory.

AIDS Vaccines↗
PubMed2006

Differentiation of memory B and T cells.

In the past few years progress has been made in understanding the molecular mechanisms that underlie the initial generation, and the ensuing differentiation and maintenance, of humoral and cellular immunity. Although B and T cell immunological memory contribute to protective immunity through fundamentally distinct effector functions, interesting analogies are becoming apparent between the two memory compartments. These include heterogeneity in function, anatomical location and phenotype, which probably relate to differential environmental cues during the early priming events as well as the later differentiation phases. Detailed definition of the molecular and cellular signals involved in the development of immunological memory, and the relative contributions of different memory subsets to protective immunity, remains an important goal.

Animals↗
PubMed2002

Pneumococcal vaccination of children.

Streptococcus pneumoniae is the most frequent cause of invasive bacterial infection in children younger than 2 years of age, reaching a peak incidence at 6 to 12 months of age. Pneumococci also cause many cases of pneumonia, sinusitis, and otitis media. Incidence rates of invasive infection in children with sickle cell disease, acquired or congenital splenectomy, or human immunodeficiency virus infection are 20- to 100-fold higher than are those of healthy children during the first 5 years of life. Other healthy children, such as those of American Indian, Native Alaskan, or African American descent, also have high rates of invasive infection, and those children enrolled in out-of-home care may have modestly increased risks. Pneumococcal polysaccharide polyvalent vaccines have been available for more than 2 decades but are limited in their usefulness for children because of their inability to induce protective antibody responses in children younger than 2 years of age and lack of immunologic memory. In contrast, pneumococcal protein conjugate vaccines induce presumptive protective responses in infants younger than 6 months, and immunologic memory further enhances responses after booster doses are given. Currently, a single heptavalent pneumococcal protein conjugate vaccine is licensed for use in the United States and is recommended for routine administration to all children, beginning at 2 months of age. It also is recommended for children between 24 and 59 months of age who are at high risk of acquiring invasive disease.

Child↗
PubMed2005

Anamnestic responses of mice following Mycobacterium tuberculosis infection.

The anamnestic response is the property of the immune system that makes vaccine development possible. Although the development of a vaccine against Mycobacterium tuberculosis is an important global priority, there are many gaps in our understanding of how immunological memory develops following M. tuberculosis infection or after BCG vaccination. In experiments designed to compare the anamnestic response of susceptible and resistant mouse strains, major histocompatibility complex-matched memory-immune C3.SW-H2(b)/SnJ and C57BL/6 mice both demonstrated better control of bacterial replication following reinfection with M. tuberculosis than control mice. Nevertheless, this memory response did not appear to have any long-term protective effect for either mouse strain. A greater understanding of the immunological factors that govern the maintenance of immunological memory following exposure to M. tuberculosis will be required to develop an effective vaccine.

Animals↗
PubMed1991

A possible site of in vivo action of cyclosporin A for transplantation immunity: comparative study with cyclophosphamide.

The immunosuppressive mechanisms of cyclosporin A (CsA) and cyclophosphamide (CPM) in vivo were studied by measuring the transplantation immunity for second set rejection of an allogeneic ascites tumor. The transplantation immunity in our assay system was mediated primarily by allospecific cytotoxic T lymphocytes (CTL). Our results showed that both CsA and CPM did not affect the process of inducing the immunity, but they inhibited the effector phase of that transplant immunity. The experiments using 51Cr-release assay in vitro on peritoneal exudate cells as effector cells showed that the effector phase of the transplantation immunity in vivo involved the maturation from immunological memory CTL-precursor cells to effector CTL with clonal expansion. Further, adoptive cell transfer experiments showed that CsA did not eliminate the immunological memory CTL nor induce the suppressor cells in donor mice. All the data suggested that the maturation of memory CTL precursor cells to effector CTL was inhibited by CsA which would block lymphokine production even in vivo, whereas CPM eliminated the CPM-sensitive memory CTL precursor cells. The findings that CsA and CPM act on the different sites of CTL maturation support the possibility of effectiveness of the combination therapy of the two agents for controlling the transplantation immunity.

Animals↗
PubMed1982

Antigen content of inactivated poliovirus vaccine for use in a one- or two-dose regimen.

The immunologic response to inactivated poliovirus vaccine following one and two doses has been studied in infants in developing and developed countries using vaccine prepared at the Rijks Instituut voor de Volksgezondheit, The Netherlands. Virus was grown in microcarrier cultures of monkey kidney cells, purified, concentrated, and inactivated with formalin. The vaccines used contained different quantities of D-antigen units for each of the three types. The data reveal that both antibody and immunologic memory (booster-type responsiveness) were induced in virtually all individuals following a single dose of a sufficient quantity of antigen. Immunologic memory was readily revealed by the booster-type response following a second dose given six months after the first. The degree of booster-type response to a second dose is linked primarily to the quantity of antigen used for primary immunization, and secondarily to the quantity of antigen used for the booster dose. The data base is presented for formulating the antigen content of an inactivated poliovirus vaccine that can be relied upon to be protective after the first dose when given alone or when incorporated with combinations of other antigens (diphtheria-per tussis-tetanus) that may require two or more doses.

Antibody Formation↗
PubMed1986

Neuroimmunomodulation: impairment of humoral immune responsiveness by 6-hydroxydopamine treatment.

Previous studies from this laboratory and others show that perturbations of the central nervous system modulate immune function. In addition, reports from several investigators indicate that depletion of the neurotransmitter norepinephrine (NE) in peripheral nerves by injecting the neurotoxin 6-hydroxydopamine (6-OHDA), can enhance or suppress the antibody response. However, immunocompetence following brain depletion of catecholamines has not been investigated. In this study, we investigated the effects of injecting 6-OHDA into the cisterna magna of male CBA/J mice, and determined the effects of this treatment on both the IgM and IgG antibody responses to sheep red blood cells (SRBC). Both responses are suppressed compared to saline-injected control or normal animals. Animals treated with 6-OHDA have decreased levels of NE in the midbrain, pons-medulla and hypothalamus, while dopamine levels did not change in these brain regions but was decreased in the striatum. The percentage of splenic T cells and B cells was not affected by 6-OHDA treatment. Although there is a marked increase in plasma corticosterone levels in 6-OHDA-treated mice, saline-injected control animals have equivalent increases in plasma corticosterone without concomitant impairment of the immune response. Thus, the decline in immune responsiveness following 6-OHDA treatment does not result from corticosterone-induced immunosuppression. Analysis of the kinetics of the primary IgG response following 6-OHDA treatment indicates that the magnitude, but not the kinetics, of the response decreases. Experiments to determine the effects of 6-OHDA on the afferent and efferent phrases of the response demonstrate that it is effective only when administered prior to immunization, and thus must inhibit early events involved in the initiation of the response. Additional experiments show that mice can be immunized 2 weeks following brain catecholamines depletion and still exhibit a decreased antibody response. However, the response returns to normal levels if immunization is delayed 4 weeks after injection. Further experiments demonstrated that 6-OHDA treatment has no effect on the secondary antibody response, but does inhibit the development of immunological memory. Collectively, these results indicate that 6-OHDA treatment has a profound inhibitory effect on the induction of the primary antibody response and immunological memory development, but is without effect on the secondary antibody response. The data further substantiate the existence of a link between the brain and the immune response.

Animals↗
PubMed1976

[Selective concurrent suppression of the process of rosette-forming cell accumulation during the immune response].

Repeated injections to mice of normal rabbit immunoglobulins preceding immunization with sheep erythrocytes inhibited the accumulation of rosette-forming cells (RFC) in the spleen, without influencing the proliferation of the antibody-forming cells and hemaggutinin production. Reduction of the RFC under these conditions occurred on account of B-cells whose antigen-binding receptors could be blocked by antibodies against the aggregated mouse immunoglobulins and a complex of polyadenylic-polyuridylic acids. Repeated injections of the competitive antigen enhanced the formation of the immunological memory to the second antigen. The problem of the origin of the immune rosette-forming B-cells and their influence on the formation on the immunological memory is discussed.

Animals↗
PubMed2006

T-cell memory and recall responses to respiratory virus infections.

The respiratory tract is characterized by its large surface area and the close association of an extensive vasculature with the external environment. As such, the respiratory tract is a major portal of entry for many pathogens. The immune system is able to effectively control most pulmonary pathogens and establish immunological memory that is capable of mediating an accelerated and enhanced recall response to secondary pathogen challenge. A key component of the recall response in the lung involves the rapid response of antigen-specific memory CD8+ T cells. Recent studies have shown that memory CD8+ T cells are extremely heterogeneous in terms of phenotype, function, anatomical distribution, and longevity. However, we have little understanding of how the different subsets of memory cells actually contribute to the recall response, especially with respect to peripheral or mucosal sites, such as the lung. Since immunological memory is the cornerstone of vaccination, it is essential that we understand how different memory CD8+ T-cell subsets are initially generated, maintained over time, and contribute to recall responses. This review focuses on memory T cells that mediate recall responses to influenza and parainfluenza virus infections in the lung.

Animals↗
PubMed1991

Abrogation of neonatally induced permanent transplantation tolerance in mice: quantitative aspects.

Neonatal transplantation tolerance was induced in CBA (H-2k) mice by the intravenous injection of 20 million (CBAxA)F1 spleen cells to the transplantation antigens of the A mouse strain. Those mice which carried an A (H-2a) skin allograft without any sign of rejection for at least 120 days, were considered to be permanently tolerant and were selected for further experiments. Abrogation of permanent transplantation tolerance was achieved by injecting the tolerant mice with different doses (50, 100 and 200 millions, respectively) of normal syngeneic (CBA) lymphoid (spleen) cells. Dynamics of the rejection of the test skin allografts tolerated so far revealed well reproducible dose-response curves. Further groups of tolerant CBA mice were given 10, 50, 100, or 200 million "sensitized" (G + 16) CBA spleen cells: "sensitization" by A-skin allografting was performed 16 days before. The sensitized spleen cells abolished the state of tolerance more vigorously and effectively than the normal CBA spleen cells did. In a third group of experiments, the abrogating capacity of 50 million sensitized CBA spleen cells 16, 120, 240, or 360 days after sensitization was compared. The efficacy of the sensitized cells in abolishing the state of tolerance decreased continuously, but, even 360 days after sensitization a remarkably strong immunologic memory was demonstrable. The excellent quantitative correlations found between the number of the injected lymphoid cells and the dynamics of the abrogation of tolerance offer a highly promising new possibility for studying the immunological activity, the immunologic memory, etc., of the different lymphoid cell (sub)populations in performing the transplantation immune reactions.

Animals↗
PubMed2004

Long-term persistence of immunity to hepatitis B after vaccination during infancy in a country where endemicity is low.

BACKGROUND: The long-term response to hepatitis B vaccination during infancy has not been fully evaluated in countries where endemicity is low. METHODS: The present study was a serological investigation of immunity to hepatitis B during adolescence. In a cohort of children who were born to hepatitis B virus carrier mothers and who were vaccinated during infancy, evidence of past or current infection and the response to a single booster dose of vaccine were analyzed. Sixty-four children whose antibody levels were measured after immunization (group 1) and 52 younger siblings who did not undergo postvaccination antibody tests (group 2) were studied. RESULTS: One child in each group showed evidence of natural infection. In group 1, 32 children (50%) had undetectable antibody to hepatitis B surface antigen (anti-HBs), and only 8 (13%) had levels >100 mIU/mL. After a booster dose of vaccine, only 7 (11%) still had undetectable anti-HBs, 3 (5%) showed a primary response, and 50 (78%) had levels >100 mIU/mL. Five of the 7 vaccine nonresponders and all of the primary responders had also received hepatitis B-specific immunoglobulin (HBIG) at birth. The children in group 2 showed a similar response to the vaccine, but with slightly higher levels of anti-HBs. CONCLUSIONS: Most children vaccinated at birth retain immunological memory to hepatitis B vaccine for 15 years, but those who did not were more likely to have received HBIG at birth, suggesting that passive antibody may interfere with the induction of immunological memory.

Adolescent↗
PubMed1997

Adoptive transfer of anti-CD3-activated CD4+ T cells plus cyclophosphamide and liposome-encapsulated interleukin-2 cure murine MC-38 and 3LL tumors and establish tumor-specific immunity.

The infusion of anti-CD3-activated murine T cells plus interleukin-2 (IL-2) exerts antitumor effects against several tumors in murine immunotherapy models. This study compares the therapeutic efficacy of anti-CD3-activated CD4+ or CD8+ T-cell subsets, when given with cyclophosphamide (Cy) and liposome-encapsulated IL-2 (L-IL2) in a murine model. C57BL/6 mice bearing subcutaneous (S.C.) MC-38 colon adenocarcinoma, 3LL Lewis lung carcinoma, or 38C13 lymphoma for 7 to 14 days were pretreated with low-dose intraperitoneal (I.P.) Cy before intravenous (I.V.) injection of anti-CD3-activated T cells or T-cell subsets. Cell administration was followed by I.P. administration of L-IL2 for 5 days. Mice receiving activated CD4+ T cells showed significantly reduced tumor growth or complete remissions with prolonged disease-free survival in MC-38, 3LL, and 38C13. The timing of Cy doses in relation to adoptive transfer was critical in obtaining the optimal antitumor effect by CD4+ cells. Injecting Cy 4 days before the infusion of CD4+ cells greatly enhanced the antitumor effect of the CD4+ cells and improved survival of the mice compared with other Cy regimens. C57BL/6 mice cured of MC-38 after treatment with CD4+ T cells developed tumor-type immunologic memory as demonstrated by their ability to reject rechallenges with MC-38, but not 3LL. Similarly, mice cured of 3LL tumors rejected rechallenges of 3LL, but not MC-38. The immunologic memory could be transferred with an I.V. injection of splenocytes from mice cured of MC-38 or 3LL. No cytotoxic T-lymphocyte activity was detected in T cells or T-cell subsets from mice cured of MC-38 or 3LL. Increased IL-2 and interferon-gamma (IFN-gamma) production was observed from CD4+ subsets in cured animals when stimulated in vitro with the original tumor, but not with an unrelated syngeneic tumor. These results suggest that tumor-specific immunity can be achieved in vivo with anti-CD3-stimulated CD4+ T cells in this cellular therapy model.

Adenocarcinoma↗
PubMed2005

Partial, but not complete, tumor-debulking surgery promotes protective antitumor memory when combined with chemotherapy and adjuvant immunotherapy.

Resection alone is rarely curative for advanced tumors, but the outcome generally improves with adjuvant therapy. We have previously shown that a combination of traditional chemotherapy (gemcitabine) and immunotherapy (anti-CD40/FGK-45) without surgery is synergistic and can lead to long-term cure when applied to small tumors. Such cured animals have immunologic memory and are protected from rechallenge. Here we investigate the effectiveness of combination chemotherapy and immunotherapy after partial or complete surgical debulking of large tumors. We found that complete resection followed by combination chemotherapy/immunotherapy led to a high rate of cure (>80%) but failed to induce a long-term, tumor-specific memory. Partial debulking followed by combination therapy elicited the same proportion of cured animals but in contrast to complete resection, a memory response was invoked. We postulate that chemotherapy induced apoptosis of the residual tumor cells following incomplete resection is absolutely required for the induction of long-term immunologic memory.

Animals↗
PubMed1990

[The role of T-lymphocytes in the development of a humoral immune response to the corpuscular antigen of Staphylococcus aureus].

The dependence of humoral immune response and the formation of immunological memory to corpuscular staphylococcal antigen (CSA) on the T-system of immunity was studied in experiments on B-mice and on mice with the congenital absence of the thymus (nude). Primary and secondary immune response to CSA in athymic mice was found to be considerably less than in normal animals. After the repeated immunization of genetically athymic mice the pronounced secondary reaction of the formation of antibodies to CSA was observed. As shown in this investigation carried out with the use of adoptive transfer techniques, the induction of memory B-cells to CSA may occur in animals with congenital or experimentally induced T-immunodeficiency. The conclusion was made on the T-dependence of humoral immune response to CSA, the formation of immunological memory to this antigen being relatively T-independent.

Animals↗