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Results for “Immunologic Memory”

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At least 1,351 records · Page 75Linked to original sources
PubMed1998

CD40 ligand is pivotal to efficient control of virus replication in mice infected with lymphocytic choriomeningitis virus.

CD40 ligand (CD40L) is an important molecule that is known to be involved in T-B collaboration and certain aspects of cell-mediated immunity. However, its role in antiviral immunity has not been clearly defined as of yet. Therefore, mice with a targeted defect in the gene encoding this molecule were infected with one of two strains of lymphocytic choriomeningitis virus differing markedly in their capacity to spread in the host. Infection with lymphocytic choriomeningitis virus is initially controlled primarily by CD8+ effector cells, whereas long-term immune surveillance also depends upon CD4+ cells and B cells. Our results reveal that the primary activation, clonal expansion, and differentiation of CD8+ T cells does not require expression of CD40L. However, lack of expression results in rapid impairment of CTL responsiveness and failure to permanently control virus replication. This happens not only in mice infected with the rapidly spreading virus strain but also at a late stage in mice infected with the strain of more limited potential for spreading. In the latter mice, virus replication is initially controlled very efficiently, but high levels of virus can be detected in the blood and internal organs approximately 6 mo after virus inoculation. Since the impairment of immune function seems to be more pronounced in CD40L-deficient mice than in mice lacking either CD4+ cells or B cells, these results indicate that CD40L is pivotal to sustain efficient antiviral immune surveillance, including CD8+ T cells, and suggest that CD40L is critically involved in cellular interactions in addition to T-B cooperation.

Animals↗
PubMed1998

Lack of in vitro lymphoproliferative response to hepatitis B surface antigen in healthy vaccine recipients.

A majority of HBsAg vaccine recipients show good anti-HBs antibody responses but poor antigen specific lymphoproliferative responses. We investigated the basis for this poor in vitro antigen specific proliferative responsiveness in vaccinees who had received the standard three dose schedule (0, 1 and 6 months) of plasma derived HBsAg vaccine. Peripheral blood mononuclear cells (PBMC) from 26 of 29 (89.7%) vaccinees failed to show lymphoproliferative responses to HBsAg in spite of having a very good anti-HBs antibody response (geometric mean titre 3154 IU/1). The mitogen (phytohaemagglutinin, PHA) and antigen (purified protein derivative, PPD) driven lymphoproliferative responses in these individuals were normal. Addition of exogenous recombinant interleukin-2 (rIL-2) along with HBsAg had no effect in the response to HBsAg in six of nine vaccinees, who were tested six months after the third vaccine dose or in four unvaccinated controls. However, in three vaccinees who did not have lymphoproliferative response to HBsAg alone, addition of exogenous rIL-2 resulted in a synergistic response. These data suggest that HBsAg reactive cells are few in the peripheral circulation of a majority of individuals following the standard three dose schedule of vaccination and addition of exogenous rIL-2 induces a response only in a subgroup of individuals. The inability of HBsAg to induce a T cell proliferative response may have implications for the maintenance of protective immunity and immunological memory following vaccination.

Adult↗
PubMed1976

[Immunological aspects of corticotherapy].

The therapeutic effectiveness of corticoids in transplantation, in autoimmune conditions and in numerous diseases in which the pathogenic role of hypersensitivity reactions is invoked, is perfectly established on the empirical basis of clinical cases. The study of the effects of corticoids on the immunological response is on the contrary very fragmentary; it comes up against numerous difficulties, especially against the differences in susceptibility from one species to another. The lymphoid cells have cytoplasmic and nuclear receptors for corticosteroids. The fixation of corticosteroids on lymphocytes inhibits the synthesis of nucleic acids and raises the intracellular level of cyclic AMP. Corticosteroids decrease the mobility of polymorph leukocytes in the presence of a chemotactic stimulus, at high doses, they disturb phagocytosis by marcophages, oppose the degranulation of mast cells and polymorph leukocytes, and the cytotoxic action of sensitised T lymphocytes. In vivo, corticosteroids have little effect on the production of antibodies (primary of secondary response) do not modify the "immunological memory" by through an anti-inflammatory effect, abolish the peripheral manifestations of late hypersentsitivity reactions. Corticosteroids enable the treatment of acute rejection crises in transplantation, they have a symptomatic effect on type I and IV Gel and Cooms hypersensitivity reaction, their activity is less regular in the other phenomena of hypersensitivity.

Adrenal Cortex Hormones↗
PubMed1976

[Globulin producing cells in cultures of blast-transformed lymphocytes in vitro].

Globulin-producing cells -- lymphocytes, transitional transformed forms, blasts and plasmocyte-like cells were revealed with the aid of Coon's method in the culture of the human peripheral blood following stimulation with staphylococcus filtrate and phytohemagglutinin. Analysis of dynamics of the appearance of these cells suggests that they originate from a special B-lymphocyte subpopulation -- the immunological memory cells. Some of the globulin-producing cells arose from precursors without any division, in others differentiation was combined with proliferation.

Adult↗
PubMed1999

Eradication of rat malignant gliomas by retroviral-mediated, in vivo delivery of the interleukin 4 gene.

Overexpression of interleukin 4 (IL-4) can impair the tumorigenicity of glioma cells, but direct evidence of its antitumor efficacy after in vivo gene transfer into malignant gliomas has not been provided. To test this, we first injected into the brain of Sprague Dawley rats a 1:1 mixture of C6 rat glioblastoma cells and psi2.L4SN20 or E86.L4SN50 retroviral producer cells (RPCs), secreting 20 and 50 ng of IL-4/5 x 10(5) cells/48 h, respectively. Twenty-seven and 56% of rats receiving injections with these low- or medium-level IL-4 RPCs, respectively, survived tumor injection, whereas control rats died in about 1 month. E86.L4SN50 RPCs coinjected with 9L gliosarcoma cells into syngeneic Fischer 344 rats yielded similar results. A novel IL-4 RPC clone expressing higher levels of IL-4, E86.L4SN200, coinjected with 9L cells increased to 75% the fraction of long-term survivors and induced tumor regression in 50% of rats when injected into established 9L gliosarcomas. Cured rats developed an immunological memory because they rejected a challenge of wild-type 9L cells into the contralateral hemisphere. Magnetic resonance imaging was used to monitor 9L and C6 gliomas and gave direct evidence for tumor rejection in treated rats. Immunohistology showed inflammatory infiltrates in IL-4-treated tumors in which CD8+ T lymphocytes were more abundant, although CD4+ T lymphocytes, B lymphocytes, and macrophages were also present. Overall, these findings suggest that IL-4 gene transfer is a new, promising approach for treating malignant gliomas.

Animals↗
PubMedDate not supplied

[Interrelationship between immunologic and neurologic memory: learning ability of rats during immunostimulation].

Studies have been made on the effect of an immunostimulator - the complete Freund's adjuvant - upon the learning ability in Wistar rats for visual discrimination using food-obtaining and avoidance of the electric shock techniques. Injection of the adjuvant significantly increases learning ability provided negative reinforcement technique is used, but inhibits the former under the conditions of positive reinforcement. Analysis of the extinction of the conditioned reflexes yielded similar results. Possible relation of immunogenesis to the formation of memory is discussed.

Animals↗
PubMed1978

Optimal strategies in immunology. II. B memory cell production.

After a first encounter with most antigens, the immune system responds to susequent encounters with a faster, more efficient and more strenuous antibody response. The memory of previous antigen contacts is carried by lymphocytes. Expanding on the model developed in Part 1 of this paper, we examine the optimal strategy available to the immune system for B memory cell production. We again find that the strategy should be of the bang-bang variety. The model we consider assumes that antigen triggers a subpopulation of B-lymphocytes. These triggered lymphocytes can proliferate and secrete modest amounts of antibody, or differentiate into non-dividing plasma cells which secrete large amounts of antibody, or differentiate into non-antibody secreting memory cells. Given injections of antigen at two widely spaced times we compute the strategy which minimizes a linear combination of the primary and secondary response times. We find that for all biologically reasonable parameter values the best strategies are ones in which memory cells are produced at the end of the primary response. Exerimental results which bear on the actual strategies employed are discussed.

Antibody Formation↗
PubMed1995

On the cellular basis of immunological T cell memory.

We have studied memory in T cell receptor (TCR) transgenic mice expressing a Db-restricted TCR specific for the male peptide (H-Y). CD8+ T cells from female TCR transgenic C57BL/6 (B6) mice were activated by transferring them into X-irradiated male (B6 x bm12)F1 hybrid recipients. Subsequently, they were highly purified by cell sorting and transferred for various lengths of time into female B6 nu/nu recipient mice. Other nu/nu recipient mice received highly purified naive T cells expressing the transgenic TCR. The functional potential of naive and "memory" T cells was analyzed by stimulation with male cells in vivo. The results show that memory cells can be derived from activated T cells and persist in the absence of antigen for at least 13 weeks. Naive and memory T cells differ in that memory T cells give a more vigorous and sustained response than naive T cells.

Animals↗
PubMed1977

Immunological specificity and memory in a scleractinian coral.

Tissue transplantation immunity with a specific memory component is demonstrated in populations of Montipora. This highly discriminating immunoreactivity derives from extensive allogeneic polymorphism of histocompatibility (H) markers. An H system of immunorecognition is postulated to have originated in multicellular invertebrates probably beginning with coelenterates.

Animals↗
PubMed1984

Serum antibodies after vaccination with Haemophilus influenzae type b capsular polysaccharide and responses to reimmunization: no evidence of immunologic tolerance or memory.

Haemophilus influenzae type b capsular polysaccharide vaccine was given in Finland in 1974 to approximately 50,000 infants and children, whose serum anti-H influenzae type b capsular polysaccharide levels have been followed for 3 1/2 years. The serum antibodies induced by the vaccination proved short-lived (less than 6 months) in the infants younger than 18 months. Elevated serum antibody levels were detectable for 1 1/2 years but less than 3 1/2 years in the children who were vaccinated when 18 to 35 months old. In the children who were 3 to 5 years old when vaccinated, the elevated anti-H influenzae type b capsular polysaccharide levels persisted for at least 3 1/2 years. Therefore, children vaccinated at the age of 18 months may need a new dose of vaccine 1 to 1 1/2 years after the first dose in order to be protected for the period of high susceptibility, until the age of approximately 7 years. Some of the vaccinated children were reimmunized 3 1/2 years after the first dose, and the anti-H influenzae type b capsular polysaccharide levels in their sera were studied in a similar manner. At no time did the anti-H influenzae type b capsular polysaccharide levels after the reimmunization differ from the anti-H influenzae type b capsular polysaccharide levels seen after the first vaccination in children of the same age.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗
PubMed1979

Teeth transplanted across a multiple non-H-2 barrier stimulated weak cell-mediated immunity without memory.

The genetic and immunologic criteria required for successful tooth transplantation have yet to be defined. Teeth grafted across strong barriers elicit vigorous immunity. However, teeth and tooth germs transplanted to subcutaneous sites in H-2 compatible but multiple-non-H-2 disparate recipients stimulated weak in vitro cellular cytotoxicity compared with skin grafts 5 mm in diameter. Furthermore, tooth allografts did not sensitize recipients as measured by the rejection of second-set, donor skin grafts. It may be that tooth allografts provoke fewer detrimental immune mediator systems than do skin grafts across moderate to weak transplantation barriers.

Animals↗
PubMed1994

The Dale E. McFarlin Memorial Lecture: the immunology of the multiple sclerosis lesion.

This review surveys the structural terrain of the multiple sclerosis (MS) lesion from the standpoint of its immunologic responsiveness. Similarities in lymphocyte trafficking patterns are noted between MS and its laboratory model, experimental allergic encephalomyelitis (EAE), and in both conditions, the inflammatory response is selective for the central nervous system (CNS). While adhesion molecules abound during the genesis of the MS lesion, none has yet been found that is unusual to this condition and, indeed, many occur in other neurodegenerative states in which inflammation is not a component of the lesion. Cytokines are effective regulators of lymphocyte traffic and adhesion events and most can be located in MS lesions. Of these, tumor necrosis factor-alpha (TNF-alpha) occurs in abundance. Together with its known affinity to effect myelin and oligodendrocyte destruction and to up-regulate adhesion molecule expression, the presence of TNF-alpha renders it an important player in lesion pathogenesis. Demyelination is described as a rapid lytic event, perhaps involving cytokines and immunoglobulin, and structural similarities are common in the patterns seen in MS and EAE. Oligodendrocytes survive the initial stages of lesion formation. Moreover, they are now known to proliferate and elaborate new myelin at the same time as myelin is being degraded. This paradoxical reparatory scenario is apparently a transient event although rims of remyelination persist about the margins of chronic lesions. The speculation is reiterated that the demise of the oligodendrocyte in MS may occur late in lesion formation and may be in part related to the expression of heat shock proteins (specifically, members of the hsp 60 family), potent stimulators of T-cell receptor-gamma delta T cells that have been claimed to have cytolytic activity and that have been located in chronic active MS lesions. In sum, while no single immune system molecule can be assigned as unusual to the CNS in MS, and while there appears to be nothing unique about the manner in which the CNS responds to the inflammation, the true uniqueness of the situation in MS is probably related to the many, normally sequestered, specific antigens within the myelin sheath and the biology of the myelinating cell, the oligodendrocyte.

Animals↗
PubMedDate not supplied

Relations between immunological and neurological memory: learning ability in rats during immunostimulation.

The effect of an immunostimulator, Freund's complete adjuvant (FCA), on the ability of Wistar rats to learn in a visual discrimination test was studied by foodgetting and electric-shock avoidance methods. A significant improvement in learning ability was demonstrated under the influence of FCA when the negative reinforcement method was used, but a worsening when the positive reinforcement method was used. Analysis of the dynamics of extinction of the reflexes formed gave similar results. The possible relations between immunogenesis and memory forming processes are discussed.

Animals↗
PubMed2005

Impaired recall of CD8 memory T cells in immunologically privileged tissue.

Foreign Ags that enter immunologically privileged sites such as the eye, brain, and testis persist for an extended period of time, whereas the same Ags are rapidly eliminated at conventional sites. Immune privilege, therefore, provides unwanted refuge for pathogens and tumor cells but is beneficial for the survival of allogeneic grafts. In this study, we asked whether memory T cells can eliminate foreign Ags deposited at an immunologically privileged site by studying CD8 memory T cell-mediated rejection of pancreatic islet allografts placed either in the testis (a privileged organ) or under the kidney capsule (a nonprivileged site) of diabetic mice. We found that CD8 memory T cells reject intratesticular grafts at a significantly slower rate than the rejection of intrarenal grafts. Delayed graft rejection in the testis was not due to reduced homing or proliferation of memory T cells but due to their increased apoptosis at that site. Apoptosis was mediated by the combined actions of two TNFR family members that are up-regulated on activated memory T cells, Fas, and CD30. Therefore, memory T cells survey immunologically privileged tissues but are subject to the immunosuppressive mechanisms present at these sites.

Animals↗
PubMed2006

Specificity and plasticity of memory lymphocyte migration.

To exert immunological activity, T and B cells must leave the blood and enter different extravascular compartments in the body. An essential step in this process is their adhesion to microvascular endothelium and subsequent diapedesis into a target tissue. Naive and effector/memory T and B cells possess distinct repertoires of traffic molecules that restrict their ability to interact with specialized microvessels in different anatomic compartments and thus exhibit distinct patterns of migration. In addition, antigen-experienced lymphocytes are subdivided into different subsets based on their expression of characteristic sets of adhesion receptors that favor their accumulation in certain target organs, such as the skin and the gut. This article focuses on recent discoveries that have broadened our understanding of the "imprinting" mechanisms responsible for the generation of tissue-specific effector/memory lymphocytes, especially in the intestine. We discuss how gut-specific homing is acquired, maintained, and modulated and how these mechanisms might be harnessed to develop improved vaccine protocols and treatments for intestinal autoimmune diseases.

Animals↗