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Results for “Immunologic Memory”

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At least 1,621 records · Page 90Linked to original sources
PubMed1998

A model of primary HIV-1 infection.

We construct a model based on biological principles of the interaction of HIV-1 with the CD4+ T cells at primary infection. Most of the parameters are obtained from the literature, the remainder from fitting the output of the model to data from seven patients. On the basis of the model we find that initial viral containment is due to an effective immune response. The viral level after the initial peak, a surrogate marker of disease progression, was determined by the rate of reactivation of memory cells. Differences in this rate may occur because of inter- or intra-individual differences in the capability of memory cells to recognise and dispose of variants of HIV, either due to immune escape mutations within the virus or because the virus directly inhibits reactivation. With no choice of parameters could direct and indirect killing produce the gradual loss in CD4+ T cells with the observed viral behaviour. The loss of CD4+ T cells is perhaps due to defective expansion of activated cells of both HIV specific and nonspecific cells. As less memory cells are produced as a result then this compartment decreases and hence so do naive numbers through less reversion of memory cells to the naive phenotype.

Adult↗
PubMed1999

The disappearing CD4(+)T cells in HIV infection: a case of over-stimulation?

Infection with the human immunodeficiency virus (HIV) causes a gradual decline in essential immune-system cells called CD4(+)"helper" T cells. These cells are also principal viral targets, but, paradoxically, direct cell-killing does not explain their disappearance. HIV also induces a chronic and increasing state of immune activation. In a mathematical model of normal T-cell kinetics incorporating a cytokine growth factor, increased activation alone explains these T-cell losses, a switch from "naïve" to "memory" phenotype, and certain other features of HIV disease.

CD4-Positive T-Lymphocytes↗
PubMed2006

Lysine methylation and 'signaling memory'.

A combination of various post-translational modifications regulates the formation of signaling networks in both the nucleus and the cytosol. Of these, lysine methylation provides a relatively stable marker on histones and contributes to the formation of a distinct pattern of histone-dependent gene regulation ('transcriptional memory'). Thus far, lysine methylation was considered to be nucleus specific; however, recent findings indicate that lysine methylation contributes to receptor-mediated signal transduction in the cytosol.

Animals↗
PubMed1978

Idiotype-specific T helper cells are required to induce idiotype-positive B memory cells to secrete antibody.

We have tested the proposition that induction of certain sets of B cell clones to produce antibody requires a signal from T helper cells that recognize idiotypic determinants expressed on Ig receptors of the relevant B cell clones. The approach is based on the analysis of T cell populations required to induce B cells to secrete anti-arsonate antibodies that are marked by a cross-reactive idiotype (CRId). crid+ anti-azophenyl arsonate (Ar) antibodies are produced in A/J strain mice after immunization with Ar keyhole limpet hemocyanin and represent 20--70% of the total anti-Ar antibody response. These studies indicate that antibody secretion by idiotype+ B memory cells requires two signals: one provided by "carrier"-specific Ly-1 cells, and a second delivered by idiotype-specific Ly-1 cells. Both signals are required for optimal induction of idiotype+ B memory clones.

Animals↗
PubMed1995

Life span of naive and memory T cells.

The life span of mature T cells is reviewed. Peripheral T lymphocytes are a heterogeneous population and comprise a mixture of naive, effector and memory cells. The recirculating pool of mature T cells is formed during young life through gradual release of naive T cells from the thymus. In adults, the pool of mature T cells is relatively self-sufficient, and input of new T cells from the thymus declines to low levels. Studies on T cell turnover indicate that most peripheral T cells can remain in a resting state for long periods (months in rodents and years in humans). Examination of the phenotype of dividing versus nondividing cells suggests that typical naive T cells are long-lived resting cells whereas the majority of effector and memory T cells have a much more rapid turnover. However, some memory T cells appear to divide very infrequently and eventually return to a resting state. The factors controlling the generation and maintenance of memory T cells are discussed.

Animals↗
PubMed1997

Similar ligand densities required for restimulation and effector function of cytotoxic T cells.

This study compared ligand densities on antigen-presenting cells (APCs) needed for in vitro restimulation of in vivo primed T cells and for in vitro assessed T cell effector function. Spleen cells of lymphocytic choriomeningitis virus (LCMV)-primed mice were restimulated in vitro with graded amounts of virus-derived peptides using macrophages or a cloned dendritic cell line as APCs. To test for effector function of these cytotoxic T cells, the same APCs pulsed with graded amounts of the peptides were used as target cells in an in vitro 51Cr release assay. The same peptide concentration that rendered an APC restimulatory for primed cytotoxic T lymphocytes (CTLs) also rendered it susceptible for lysis by the same CTLs. In addition, the same peptide concentrations that made macrophages susceptible for CTL-mediated lysis induced proliferative responses in vitro of in vivo primed memory CTLs. Thus, restimulation of in vivo primed T cells--measured by either proliferation or cytotoxic effector function--or sensibilization of target cells for lysis requires similar ligand densities on APCs and is therefore, contrary to expectations, governed by similar overall avidity thresholds. These results have implications for CTL memory.

Amino Acid Sequence↗
PubMed1978

Antigen requirements for induction of B-memory cells: studies with dinitrophenyl coupled to T-dependent and T-independent carriers.

Mice were primed with dinitrophenyl (DNP) (trinitrophenyl, TNP) coupled to thymus-independent (TI) or thymus-dependent (TD) carriers. B cells from these mice were transferred to irradiated recipients with T cells from keyhole limpet hemocyanin (KLH)-primed mice. After secondary immunization with DNP-KLH a significant DNP-specific IgG memory response was produced only by mice which received B cells which had been primed with TD antigens. TI antigens were unable to induce differentiation of B-cell precursors to IgG producing memory B cells but they did not suppress the induction of B-memory cells by TD antigens. The results indicate that TI antigens fail to activate a cell type which is required for the induction of memory B cells.

Animals↗
PubMed1984

Generation and decay of the immune response to a progressive fibrosarcoma. II. Failure to demonstrate postexcision immunity after the onset of T cell-mediated suppression of immunity.

This study shows that surgical removal of the meth A fibrosarcoma from its semisyngeneic host fails to result in postexcision immunity to growth of a tumor implant unless the host already has acquired a mechanism of concomitant immunity to growth of an implant. Therefore, tumor excision does not cause immunity to be generated but preserves a mechanism of concomitant immunity that already exists and which otherwise would eventually undergo down-regulation under the influence of suppressor T cells. Removal of the tumor after it has grown large enough to cause the T cell-mediated suppression of concomitant immunity does not result in the reemergence of immunity. Instead, the host remains unable to generate concomitant immunity to a second tumor for a long period of time and retains, for at least 31 d, suppressor T cells able to passively transfer suppression to appropriate recipients. Like the suppressor T cells responsible for active suppression of concomitant immunity, the suppressor T cells responsible for "memory" suppression are of the Ly-1+2- phenotype. The results indicate that progressive tumor growth results in a state of immunological tolerance of tumor-specific, transplantation antigens that can persist in the apparent absence of tumor antigens.

Animals↗
PubMed1995

Both dendritic cells and memory T lymphocytes emigrate from organ cultures of human skin and form distinctive dendritic-T-cell conjugates.

Prior studies of mouse skin in organ culture have shown that dendritic cells selectively emigrate from the explants over 1-3 d. This emigration may model the movements of dendritic cells that can occur in situ, as in transplantation and contact sensitivity. In this study, we cultured explants of normal human skin that had been removed with a dermatome. Dendritic cells with characteristic morphology and mixed leukocyte response-stimulatory activity emigrated. The dendritic cells had the expected phenotype, e.g., rich in major histocompatibility complex class II and accessory molecules such as B7-1, intercellular adhesion molecule-1, and leukocyte function-associated antigen-3. Small lymphocytes also were present in the emigrated populations and proved to be T cells exclusively, almost entirely of the TcR alpha beta and memory type (CD45RAweak, CD45RO LFA-3/CD58+), with a CD4:CD8 subset ratio of about 2:1. Some of the T cells were bound tightly to the dendritic cells. These conjugates did not dissociate after exposure to trypsin or to calcium- and magnesium-free medium, or during cytofluorography. This made it possible to sort distinct populations of single dendritic cells, single T cells, and conjugates of the two cell types. Conjugates would continue to form from mixtures of separated dendritic cells and T cells in culture. Therefore, cutaneous dendritic cells and memory T lymphocytes emigrate from human skin explants, and some of these cells form distinctive conjugates that we hypothesize contribute to immunologic recall reactions.

Cell Communication↗
PubMed1992

Roles of alpha beta and gamma delta T cell subsets in viral immunity.

The current status of T-cell subset involvement in viral immunity is summarized for experimental studies in mice. The immunobiology of the normal host response is discussed, with particular reference to lymphocytic choriomeningitis (LCM) and influenza. The general impression is that CD8+ cytotoxic T lymphocytes, CD4+ TH1 cells, gamma interferon, and IL-2 are of major importance, with these different components of the immune system interacting to promote an optimal response. However, experiments with a variety of virus systems indicate that there is considerable plasticity, at least in young, adult mice. Other mechanisms often compensate if a key lymphocyte subset is absent throughout the development of the immune response. Influenza-infected mice depleted of either CD4+ or CD8+ T cells clear virus and recover, though the latter may not be true for the elimination of LCM virus. Emerging information on the involvement of gamma delta T cells in viral pneumonia is summarized, but there is as yet no understanding of the biological significance (if any) of these lymphocytes in viral immunity. The point is made that alpha beta T-cell memory to viruses is long-lived, and the need for antigen persistence to maintain such memory is questioned.

Animals↗
PubMed2006

Four distinct patterns of memory CD8 T cell responses to chronic murine cytomegalovirus infection.

CMVs are beta herpesviruses that establish lifelong latent infection of their hosts. Acute infection of C57BL/6 mice with murine CMV elicits a very broad CD8 T cell response, comprising at least 24 epitopes from 18 viral proteins. In contrast, we show here that the CD8 T cell response in chronically infected mice was dominated by only five epitopes. Altogether, four distinct CD8 T cell kinetic patterns were evident. Responses to some epitopes, including M45, which dominates the acute response, contracted sharply after day 7 and developed into stable long-term memory. The response to m139 underwent rapid expansion and contraction, followed by a phase of memory inflation, whereas the response to an M38 epitope did not display any contraction phase. Finally, responses against two epitopes encoded by the immediate early gene IE3 were readily detectable in chronically infected mice but near the limit of detection during acute infection. CD8 T cells specific for the noninflationary M45 epitope displayed a classic central memory phenotype, re-expressing the lymph node homing receptor CD62L and homeostatic cytokine receptors for IL-7 and IL-15, and produced low levels of IL-2. Responses to two inflationary epitopes, m139 and IE3, retained an effector memory surface phenotype (CD62L(low), IL-7Ralpha(-), IL-15Rbeta(-)) and were unable to produce IL-2. We suggest that immunological choices are superimposed on altered viral gene expression profiles to determine immunodominance during chronic murine CMV infection.

3T3 Cells↗