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At least 19 recordsLinked to original sources
PubMed1996

On immunological memory.

Immunological memory is a hallmark of the immune system. Evolution can teach us which effector arms of immunological memory are biologically relevant against which virus. Antibodies appear to be the critical protective mechanism against cytopathic viruses. Since these viruses cause cell damage and disease directly, particularly in the absence of an immune response, mothers protect their offspring during a critical immunoincompetent period (a consequence of MHC- restricted T cell recognition) by passive transfer of neutralizing antibodies. In contrast, CTL appear to be the crucial effector mechanism against noncytopathic viruses. Since MHC polymorphism has made vertical transmission of T cell memory impossible, immunoincompetent offspring are not, and need not be, protected against such noncytopathic viruses. During the primary response and again during secondary infection, the most important function of CTL is to eliminate noncytopathic viruses, which may otherwise cause lethal immunopathology. Increased precursor frequencies of B and T cells appear to remain in the host independent of antigen persistence. However, in order to protect against cytopathic viruses, memory B cells have to produce antibody to maintain protective elevated levels of antibody; B cell differentiation into plasma cells is driven by persisting antigen. Similarly, to protect against infection with a noncytopathic virus, CTL have to recirculate through peripheral organs. Activation and capacity to emigrate into solid tissues as well as cytolytic effector function are also dependent upon, and driven by, persisting antigen. Because no convincing evidence is available yet of the existence of identifiable B or T cells with specialized memory characteristics, the phenotype of immunological memory correlates best with antigen-driven activation of low frequency effector T cells and plasma cells.

Animals↗
PubMed2000

On immunological memory.

Immunological memory may not represent a special characteristic of lymphocytes but simply reflect low-level responses driven by antigen that is re-encountered or persists within the host. T-cell memory is important to control persistent infections within the individual host and cannot be transmitted to offspring because of MHC polymorphism and MHC-restricted T-cell recognition. In contrast, antibody memory is transmissible from mother to offspring and may function essentially to protect offspring during the phase of physiological immuno-incompetence before, at and shortly after birth. This physiological immuno-incompetence is a result of MHC polymorphism and the dangers of the graft-versus-host and host-versus-graft reaction between mother and embryo, which necessitate immunosuppression of the mother and immuno-incompetence of the offspring. One may argue therefore that immunological memory of transmissible immunological experience is the basis on which MHC-restricted T-cell recognition could develop or coevolve.

Antibodies↗
PubMed2001

Prevention of meningococcal serogroup B infections in children: a protein-based vaccine induces immunologic memory.

Immunologic memory against meningococci was studied in 177 children (100 children were 10-11 years old and 77 were 5-6 years old) 2.5 years after vaccination with hexavalent meningococcal outer membrane vesicle (OMV) vaccine or hepatitis B (HepB) vaccine. Children were revaccinated with monovalent P1.7(h),4 meningococcal OMV vaccine. Serum bactericidal antibodies (SBAs) were measured before revaccination and after 4-6 weeks. A minimum 4-fold increase in SBAs against serosubtype P1.7(h),4 was detected in 48.5% of the children after hexavalent meningococcal vaccine and in 8.9% after HepB vaccine. Of the initial responders given hexavalent meningococcal vaccine, 78% had > or =4-fold increase in SBAs against strain P1.4. Thus, immunologic memory is present in toddlers and school-aged children previously given 3 hexavalent meningococcal vaccinations. Booster vaccination with monovalent P1.7(h),4 meningococcal OMV vaccine induces a significant increase in SBAs against serosubtype P1.7(h),4 and cross-reactivity against other serosubtypes in the hexavalent vaccine.

Antibodies, Bacterial↗
PubMed1994

Regulation of immunological memory.

Immunological memory can be regulated during either its development or its maintenance phases. Controversy and confusion surround both methods of regulation, especially in the field of T-cell memory. Recent work has helped in improving our definition of 'a memory cell', but this has been complicated by another major point of contention: whether memory cells are maintained by antigens or other stimuli. Unequivocal advances have recently been made concerning the molecular events involved in memory B cell generation in germinal centers.

Animals↗
PubMed2004

Immunological memory to viral infection.

Immunological memory is defined by the ability of a host to remember a past encounter with a specific pathogen and to respond to it in an effective manner upon re-exposure. How long immunological memory can be maintained in the absence of re-infection continues to be a subject of great controversy. Recent studies on immunity following smallpox vaccination demonstrate that T-cell memory declines steadily with a half-life of 8-15 years, whereas antiviral antibody responses are maintained for up to 75 years without appreciable decline. By combining recent advances in quantitative immunology with historical accounts of protection against smallpox dating back to the time of Edward Jenner, we are gaining a better understanding of the duration and magnitude of immunological memory and how it relates to protective immunity.

Antibodies, Viral↗
PubMed2006

Protective 'immunity' by pre-existent neutralizing antibody titers and preactivated T cells but not by so-called 'immunological memory'.

The idea of immunological memory originally arose from the observation that survivors of infections were subsequently resistant to disease caused by the same infection. While most immunologists accept a special 'remembering' memory quality, we have argued previously and document here that increased resistance against re-infection, i.e. immunity, reflects low-level antigen-driven T- and B-cell responses, resulting in elevated serum or mucosal titers of protective antibodies or of activated T cells, respectively. Periodic antigen re-exposure is from within, by persisting infection (long-term) or by immune complexes (short-term), or from without, by low-level re-infections. This simple concept is supported by clinical evidence and model experiments but is often ignored, although this concept, but not so-called 'immunological memory', as defined in textbooks (i.e. earlier and better responses of a primed host), is compatible with evolutionary maternal antibody transfer of protection as well as immunity against existing infections. The concept of 'immunity without immunological remembering memory' explains why it is easy to generate vaccines against acute cytopathic infections, particularly those of early childhood, where neutralizing antibodies are the key to protection, because it has been validated by adoptive transfer of maternal antibodies. It also explains why we have not succeeded (yet?) to generate truly protective vaccines against persisting infections, because we cannot imitate 'infection immunity' that is long-lasting, generating protective T- and B-cell stimulation against variable infections without causing disease by either immunopathology or tolerance.

Animals↗
PubMed1977

Effects of the number of DNP groups on dinitrophenylated human serum albumin upon the induction of immunological memory for the dinitrophenyl determinant.

Immunological memory to the DNP determinant is shown to be a positive correlate of the primary anti-DNP response and of the extent of DNP substitution in the priming antigen. Antigen dose-response curves for immunological memory first increase with antigen dose to reach a maximum and then decrease in the high dose region. Increasing the extent of DNP substitution in the priming antigen shifts the dose-response curves to lower antigen doses and promotes the antigen's ability to induce immunological memory to a level greater than that expected by its ability to induce a primary response. The findings are interpreted in terms of postulated effects of degree of DNP substitution on the binding of antigen to cell receptors.

Antibody Formation↗
PubMed2002

On differences between immunity and immunological memory.

The evolutionary benefits of immunological memory are important: whereas antibodies can be transmitted to offspring by their mother and thereby benefit the species, T cell memory may function to help the individual combat persistent infection in peripheral tissues. Although experimental immunological memory is largely maintained antigen-independently, protective immunity is antigen-dependent.

Animals↗
PubMed2006

Immunological memory is compromised by food restriction in deer mice Peromyscus maniculatus.

The immune system protects organisms against infection, but this protection presumably comes at a cost. Here, we asked whether food restriction would compromise the ability of an organism to generate an immune response on reexposure to an antigen, which would represent a functional cost of immunological memory. Immunological memory is generated when B and T lymphocytes sensitive to components of pathogens (i.e., antigens) proliferate after exposure and persist in circulation to hinder reinfection. To test the possibility that B cell memory, the component of the immune system responsible for antibody production, is expensive to maintain, secondary antibody production against a novel protein [keyhole limpet hemocyanin (KLH)] was compared in food-restricted and ad libitum-fed male deer mice (Peromyscus maniculatus). To determine whether compromised secondary antibody production was solely due to elevated corticosterone independent of resource availability, some food-restricted and ad libitum-fed mice were subjected to unpredictable, chronic (2 h/day) restraint. Mice fed 70% of their ad libitum diet 2 wk after primary antigen challenge produced approximately 95% less IgG against KLH after a second antigen challenge than mice fed ad libitum, even though all mice were fed ad libitum during the secondary antibody response period. Restraint had no effect on secondary IgG production in response to KLH, and corticosterone concentrations 1 day after food restriction did not differ between food-restricted and ad libitum-fed mice. Together, these data imply that secondary antibody responses and the benefits of immunological memory are energetically costly in this species.

Animals↗
PubMed1985

Cyclic development of immunological memory to bacterial lipopolysaccharide.

Immunological memory to the lipopolysaccharide of Escherichia coli O113 was generated in strains of inbred mice given a single subimmunogenic dose of either E. coli O113 lipopolysaccharide or the native protoplasmic polysaccharide of E. coli O113. Such memory, which only involved antibody of the immunoglobulin M class, developed in a cyclic manner that was characteristic for the strain of mice used. It involved cell proliferation as well as differentiation and persisted for at least 25 days after priming with a single injection of a subimmunogenic dose of E. coli O113 lipopolysaccharide.

Animals↗
PubMed1976

Transition in the character of immunological memory in mice after immunization. II. Memory in T and B cell populations.

Teh immunological memory in antibody response of mice to bovine serum albumin (BSA) was investigated at the level of antibody-producing cells or their precursor B cells and thymus-dependent helper T cells. Spleen cells obtained from mice previously primed with alum-precipitated BSA at various times were transferred to irradiated syngeneic mice. Spleen cells from mice immunized 8 days or 64 days before presented a high degree of adoptive secondary response, whereas the adoptive response of cells from mice immunized 2 days previously was found to be inferior even to that of unprimed spleen cells. Primed spleen cells treated with anti-mouse thymocyte rabbit serum plus complement were supplemented with normal thymus cells and the restoration of the responsiveness was examined. It was suggested that the memory was carried mainly by T cells in the earlier phases of the immunological memory (2 days or 8 days after the primary immunization). On the other hand, the immunological memory in the B-cell population was shown to grow gradually toward the later phase (later than 40 days).

Animals↗
PubMed2003

Turning immunological memory into amnesia by depletion of dividing T cells.

Immunological memory, defined as more efficient immune responses on antigen reexposure, can last for decades. The current paradigm is that memory is maintained by antigen-experienced "memory T cells" that can be long-lived quiescent or dividing. The contribution of T cell division to memory maintenance is poorly known and has important clinical implications. In this study, we directly addressed the role of dividing T cells in immunological memory maintenance by evaluating the consequences of their elimination. The specific ablation of dividing T cells was obtained by administration of ganciclovir to immune mice expressing the herpes simplex type 1 thymidine kinase suicide gene in T cells. We show that depletion of dividing T cells for 5 or 2 weeks suffices to abolish in vitro and in vivo memory responses against the male H-Y transplantation alloantigen or against lymphocytic choriomeningitis virus antigens, respectively. Similar results were obtained after the nonspecific elimination of all dividing cells by using hydroxyurea, a cytostatic toxic agent commonly used for cancer chemotherapy. This immune amnesia occurred in otherwise immunocompetent mice and despite the persistence of functional quiescent T cells displaying a "memory" phenotype. Thus, division of antigen-experienced T cells is an absolute requirement for immunological memory maintenance and the current concept of memory T cells is challenged.

Animals↗
PubMed2004

Immunological memory to viral infections.

The purpose of immunological memory is to protect the host from reinfection, to control persistent infections, and, through maternal antibody, to protect the host's immunologically immature offspring from primary infections. Immunological memory is an exclusive property of the acquired immune system, where in the presence of CD4 T cell help, T cells and B cells clonally expand and differentiate to provide effector systems that protect the host from pathogens. Here we describe how T and B cell memory is generated in response to virus infections and how these cells respond when the host is infected again by similar or different viruses.

Animals↗
PubMed2007

Maintenance of antigen-specific immunological memory through variable regions of heavy and light chains of anti-idiotypic antibody.

Immunological memory is characterized by a quick and enhanced immune response after re-exposure to the same antigen. To explain the mechanism involved in generation and maintenance of immunological memory, we had earlier proposed a hypothesis involving the relay of memory by idiotypic and anti-idiotypic B cells. The peptidomimic present in the hypervariable region of anti-idiotypic antibody was hypothesized to carry forward immunological memory. In the present work, we provide evidence supporting a role for the anti-idiotypic antibody in eliciting antigen-specific B-cell and T-cell responses. Employing the idiotypic monoclonal antibody (Ab(1)) specific for haemagglutinin (H) protein of rinderpest virus, Ab(2beta) was generated, which possesses an internal image of the H protein in the region between amino acids 527 and 556. We demonstrate that antigen-specific memory is perpetuated by immunization with Ab(2), as shown by maintenance of antigen-specific T-cell responses upon restimulation in vitro of Ab(2) immune splenocytes by antigen-presenting cells expressing H protein or pulsed with H-protein-derived peptides. We have also shown that boosting with antigen-specific anti-idiotypic B cells generates a memory response in antigen-primed mice. Evidence has been provided for the existence of an antigen-specific B-cell idiotypic network in the body that supports the perpetuation of immunological memory as proposed in the relay hypothesis.

Amino Acid Sequence↗
PubMed1979

[Depression and stimulation of immunologic memory by typhoid lipopolysaccharide and polysaccharide].

The effect of typhoid lipopolysaccharide (LPS) and polysaccharide (PS) on immunological memory in the system of IgM and IgG synthesis and rosette-forming cells was studied. When introduced into animals previously immunized with SRBC, PS stimulated, under certain conditions, immunological memory in the system of IgM synthesis and rosette-forming cells, while the injection of LPS induced only an insignificant stimulation of immunological memory. No stimulation in the system of IgG synthesis was observed after the injection of both LPS and PS. The suppression of immunological memory was noted in the animals receiving LPS as well as in those receiving PS the immunosuppressing effect produced by LPS was more pronounced.

Animals↗
PubMed1992

Cholera toxin adjuvant promotes long-term immunological memory in the gut mucosa to unrelated immunogens after oral immunization.

This study was conducted to investigate whether cholera toxin (CT), used as a mucosal adjuvant, would promote the development in mice of immunological memory to unrelated antigens administered by the oral route. We found that oral priming immunizations with keyhole limpet haemocyanin (KLH) in combination with CT adjuvant induced long-term, at least 22 months and perhaps lifelong, immunological memory in the intestinal lamina propria (LP). In contrast, oral priming immunizations with KLH alone failed to stimulate immunological memory. Moreover, memory responses in the KLH plus CT-immunized mice were elicited by antigen alone, i.e. without CT adjuvant, suggesting that once immunological memory is established in the intestinal mucosa, e.g. by oral vaccination, elicitation of secondary-type responses does not require the presence of CT and thus could result from re-encounter with specific bacterial or viral antigens in the intestine. We also found that a single priming-dose of KLH plus CT adjuvant was sufficient to stimulate long-term, antigen-specific memory in the intestinal mucosa. Finally, the ability of CT to induce immunological memory in the gut mucosa required the whole toxin and could not be achieved by using the toxoid, the cholera toxin B subunit (CTB), which lacks the adenylate cyclase/cAMP-activating property of the whole molecule. The results support the view that mucosal adjuvants, incorporated into oral vaccines, might be an effective means to achieve long-term immunological memory and protection against pathogenic micro-organisms at mucosal surfaces.

Adjuvants, Immunologic↗
PubMed1976

Transition in the character of immunological memory in mice after immunization. I. Memory for IgM and IgG antibody responses.

The immunological memory in antibody response of mice to bovine serum albumin was investigated at the level of IgM and IgG antibody-forming cells, The antigen at a dose much lower than required for eliciting a detectable level of the primary antibody response could latently activate the immune machinery to an extent adquate for specific recall, whereas higher doses of antigen were effective in evoking strong anamnestic response. The potentiality to develop the anamnestic response was found even in the latent phase of the primary antibody response and was maintained for more than 2 months. The immunological memory acquired in an early phase after the primary immunization mainly involved IgM antibody response and late memory concerned IgG response.

Animals↗
PubMed1996

Vaccine induced immunologic memory for hepatitis B surface antigen: implications for policy on booster vaccination.

This paper reviews published literature on the long-term persistence of immunologic memory for HBsAg after a course of hepatitis B vaccine and the functional significance this has for policy on booster vaccination. Several studies have shown that vaccine induced antibody (anti-HBs) specific for the surface antigen (HBsAg) of hepatitis B virus (HBV) is protective at a serum concentration of 10 milli-International Units per milliliter (mIU ml-1). When acquired passively (e.g. from hepatitis B immune globulin), susceptibility to infection returns as antibody declines. However, vaccine induces active synthesis of anti-HBs accompanied by immunologic memory for HBsAg that affords ongoing protection independent of antibody. Persistent memory over periods of 5 years or more is evident from large, rapid increases in antibody following booster vaccination, even in subjects who have lost antibody. Complementary studies, using an in vitro enzyme linked immunosorbent assay (spot-ELISA), show that the number of memory B lymphocytes able to produce anti-HBs does not diminish as the level of antibody declines. That immunologic memory provides effective immunity is suggested by serologic studies over periods of 5 years or more of vaccinees frequently exposed to HBV. Although many failed to maintain at least 10 mIU ml-1 of antibody, there have been very few clinically significant breakthrough infections. Thus, it appears unnecessary to give healthy vaccinees a booster vaccination when the level of anti-HBs falls below 10 mIU ml-1. Current studies suggest good retention of immunologic memory in healthy vaccinees over periods of 5-12 years. While additional studies will better define the limits of this phenomenon, routine booster vaccination should not be needed to sustain immunologic memory and protection within 5 years and perhaps longer after the primary vaccination series.

Hepatitis B Surface Antigens↗