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Results for “Immunologic Memory”

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At least 289 records · Page 16Linked to original sources
PubMed1983

Igh-V or closely linked gene(s) control immunological memory to a thymus-independent antigen.

Mice mount a normal primary antibody response on stimulation with the thymic-independent antigen trinitrophenylated lipopolysaccharide (TNP-LPS). Although we have previously reported the generation of functional B-memory lymphocytes to TNP-LPS, this memory response was only observed in few mouse strains. Here we have used congeneic mouse strains in an attempt to locate the genetic regions involved in the memory response. We show that genes of the major histocompatibility complex (MHC) do not have a critical role but that genes coding for the variable region of immunoglobulin heavy chains or gene(s) closely linked to them are required for memory cell induction by TNP-LPS.

Animals↗
PubMed1986

Immunological memory and lymphoblast-migration in mice infected with Hymenolepis nana.

The presence of small cells carrying memory and lymphoblast migration in C57 Bl/6N inbred mice with the intestinal parasite Hymenolepis nana were investigated. Hymenolepis nana egg-infection stimulated an enhanced accumulation of mesenteric lymphoblasts at days 3, 6 and 9 after infection; lymphoblasts accumulated selectively in the mesenteric nodes (MLN) of mice suggesting a cell-trapping effect. The migration was studied using lymphoblasts from non-infected donors. Spleen cells and MLNC collected from donor mice 30 days after a primary infection and enriched for T cells were able to transfer an adoptive immunity, by contrast unseparated cells were uneffective. This result provides preliminary evidence for the existence of T memory cells in the spleen and in the mesenteric nodes.

Animals↗
PubMed1982

Epitope-specific regulation. II. A bistable, Igh-restricted regulatory mechanism central to immunologic memory.

Antibody responses to commonly used antigens are regulated by an epitope- specific system composed of Igh-restricted elements responsible for controlling the isotype and allotype responses mounted to each of the epitopes on the antigen. Because these elements can be independently induced to either suppress or support antibody production, this system as a whole provides an effector mechanism capable of selectively controlling the amount, affinity, isotype representation, and epitope-specificity of an antibody response. Sequential immunizations with a carrier molecule and a hapten conjugated to that carrier (carrier/hapten-carrier immunization) induce suppression for IgG responses to the hapten. IgG(2a), IgG(2b), and IgG(3) responses are easily suppressed, whereas IgG(1) responses tend to be more resistant. Once induced, suppression tends to be maintained; however, repeated stimulation with the hapten (on any carrier) eventually induces antibody production, first for IgG(1) and later for the more suppressible isotypes (IgG(2a), IgG(2b), IgG(3)). Antibody production, once initiated, also tends to be maintained. Ongoing IgG antihapten responses in animals primed with a hapten-carrier conjugate can be suppressed by subsequent carrier/hapten-carrier immunization (using a different carrier molecule); however, the suppression induced under these circumstances is substantially weaker, i.e., it mainly affects the more suppressible isotypes and is only strong enough to detect clearly in about one-half the immunized animals. Thus, the initiation of antibody production impairs the subsequent induction of suppression, and the initial induction of suppression tends to prevent subsequent initiation of antibody production. This reciprocal relationship defines a bistable regulatory mechanism, i.e., one that tends to maintain its initially induced state but is capable of shifting to the alternate state when stimulatory conditions so dictate. The operation of such a mechanism permits conditions surrounding the first immunization with an epitope (hapten) to strongly influence but not absolutely determine which and how many of the anti-epitope memory B cells generated by that immunization will subsequently be expressed. Thus, epitope- specific regulation, although subordinate to mechanisms that control memory B cell development (as opposed to expression), plays a key role in determining the magnitude, affinity, and isotype representation of anamnestic (memory) responses produced in response to previously encountered epitopes.

Animals↗
PubMed1983

Relationship of germinal centers in lymphoid tissue to immunologic memory. VI. Transfer of B cell memory with lymph node cells fractionated according to their receptors for peanut agglutinin.

We isolated germinal center B cells by exploiting their high affinity for peanut agglutinin (PNA). The PNA+ and PNA- B cells, fractionated by panning on PNA-coated petri dishes, were examined for their ability to transfer memory responses to irradiated recipients at various times after priming. With such fractionated B cells from lymph nodes taken at the peak of germinal center formation, the largest response was obtained in recipients of the PNA+ B cell population. At 4 to 5 wk after priming, and 10 days after challenge with an unrelated antigen, memory responses were approximately equal in recipients of PNA+ or PNA- B cells. At 14 wk after priming, memory responses were found only in recipients of the PNA- B cell population. Memory B cells from the spleen, taken from mice primed in the footpad 8 wk earlier, were also PNA-. Finally, we show that boosting with a TNP-conjugate in the footpad, 6 mo after priming in the same footpad, induced the reappearance of marked memory responsiveness in the PNA+ B cell fraction of the draining node.

Animals↗
PubMed2001

Induction of immunological memory in baboons primed with DNA vaccine as neonates.

DNA immunization is a potential vaccination strategy for neonates and infants. We tested the ability of a prototype DNA vaccine against influenza virus to prime lasting immunity when administered to newborn non-human primates. Neonatal DNA vaccination triggered virus-specific and neutralizing antibodies of titers and persistence depending on the vaccine dose. Subsequent exposure to influenza virus, revealed significantly increased recall responses in the baboons vaccinated with DNA during the neonatal stage. The humoral and cellular responses were enhanced in the baboons primed with DNA vaccine as neonates. Thus, neonatal DNA vaccination of non-human primates triggered immune memory that persisted beyond infancy.

Age Factors↗
PubMed2003

Immunologic memory with no detectable bactericidal antibody response to a first dose of meningococcal serogroup C conjugate vaccine at four years.

Fourteen children with no detectable bactericidal antibody response to a first dose of meningococcal C conjugate vaccine at 4 years of age were given a booster dose of the same vaccine 2 years later. A rapid 1000-fold rise in postimmunization bactericidal antibody titers, a measured either 7 or 14 days later, suggested previous immunologic priming.

Antibodies, Bacterial↗
PubMed2005

Immunosuppressive effect of long-term drainage of thoracic duct on immunological memory in adult thymectomized rats.

Profound reduction of the recirculating lymphocyte pool using thoracic duct drainage (TDD), a method developed by Gowans et al, has been shown to be of limited immunosuppressive value when applied in experimental as well as in clinical settings across major histocompatibility antigen complex (MHC) differences. This limitation is due to the observation that animals, in particular mice, are normally not able to have the drainage last longer than 8 to 10 days. However, using a simple modification of TDD, we have established a long-term TDD method, ie, more than 20 days. Combining this long-term TDD with adult thymectomy, we have examined the life span of naive and memory T cells specific for the minor histocompatibility antigen H-Y in female lewis rats. Furthermore, we demonstrated that memory T cells specific for the H-Y antigen do not appear to be recirculating lymphocytes.

Animals↗