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Results for “Immunologic Memory”

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At least 1,459 records · Page 81Linked to original sources
PubMed1979

Immunocompetence in the lowest metazoan phylum: transplantation immunity in sponges.

Isografts of Callyspongia diffusa fuse compatibly, but allografts are invariably incompatible. Extensive polymorphism of cell-surface histocompatibility markers is evident. The histocompatibility barriers range from strong to weak depending on the interclonal combination, but early rejection with conspicous cytotoxic sequelae is typical. Reaction times of first-set, second-set, and third-party grafts indicate highly discriminating transplantation immunity with a specific memory component.

Animals↗
PubMed1975

Cyclophosphamide-induced immunological tolerance: recovery leads to a memory state.

Tolerance to SRBC has been induced in adult mice by the aid of cyclophosphamide, and the duration of the tolerant state has been tested by a second injection of antigen at different times thereafter. As evidenced by 19S and 7S PFC 4 days after challenge, tolerance in this model is of relatively short duration and leads spontaneously to a memory state.

Animals↗
PubMed2004

Jump-starting the immune system: prime-boosting comes of age.

A major challenge for immunologists has been the development of vaccines designed to emphasize cellular immune responses. One particularly promising approach is the prime-boost strategy, which has been shown to generate high levels of T-cell memory in animal models. Recently, several papers have highlighted the power of prime-boost strategies in eliciting protective cellular immunity to a variety of pathogens and have demonstrated efficacy in humans. Coupled with recent advances in our understanding of the mechanisms underlying the generation, maintenance and recall of T-cell memory, the field is poised to make tremendous progress. This Review discusses the impact of these recent developments on the future of prime-boost vaccine strategies.

Adjuvants, Immunologic↗
PubMed2002

The life and death of a B cell.

Regulation of apoptosis in the B cell lineage has implications for homeostasis, quality control of the antibody response, and tolerance. In this chapter we examine the different checkpoints that control life and death decisions of B cells during the antigen-independent and antigen-dependent phases of their development. We discuss the cell death mechanism involved in elimination of unwanted B cells at different stages of their development as well as the signals that trigger or repress the apoptotic process. At the steady state, before or after development of an immune response, B cell apoptosis ensures that the antigen receptor (BCR) on newly produced B cells is functional and does not recognize self-antigens with high avidity. It also ensures that the size of the peripheral B cell compartment remains constant in spite of the continuous input of B cells from the bone marrow. All these processes are controlled by the mitochondrial death pathway and are thus perturbed by overexpression of the antiapoptotic members of the bcl-2 gene family. By contrast, the death receptor pathway plays a prominent role during the antigen-dependent phase of B cell development. Three sets of membrane molecules stand as crucial regulators of B cell survival. First, the BCR which plays a central but ambiguous role. On the one hand, it triggers death of B cells that recognize self-antigens or have been exposed to repeated antigenic stimulations. On the other hand, it promotes survival of the peripheral mature B cell pool and protects activated B cells from CD95-induced killing. Second, the death receptor Fas/CD95 which is instrumental in censoring B cells activated in a bystander fashion at the initiation of the response to T-dependent antigens. It also drives elimination of low-affinity and self-reactive B cell clones that arise through the process of somatic mutations during the germinal center reaction. As such, it contributes to the affinity maturation of the antibody response. Finally, three membrane receptors (TACI, BCMA, and BAFF-R) which bind a newly discovered member of the tumor necrosis factor family named BAFF. BAFF acts specifically on peripheral B cells but its cellular targets seem to be restricted to two splenic B cell populations: (i) transitional immature B cells and (ii) marginal zone B cells, known to be responsible for the response to thymus-independent type 2 antigens. This suggests its possible implication in positive selection of peripheral B cells and in the antibacterial B cell responses.

Animals↗
PubMed1998

Bystander stimulation of T cells in vivo by cytokines.

Immune responses to infectious agents, especially viruses, are often associated with extensive proliferation of T cells and transient enlargement of the lymphoid tissues. Since the precursor frequency of T cells for specific antigen is low, the bulk of the T cells proliferating in the primary response are presumably stimulated via non-antigen-specific mechanisms, e.g. via cytokines elicited by the infectious agent concerned. Such 'bystander' stimulation of T cells occurs in mice injected with agents that elicit production of type I interferon (IFN I). Induction of IFN I in vivo causes marked stimulation of the CD44hi subset of CD8+ T cells and is prominent after injection of live viruses or products of bacteria such as lipopolysaccharide. Cytokines elicited by infectious agents may act as adjuvants during the primary response and could serve to boost the survival of long-lived memory cells.

Adjuvants, Immunologic↗
PubMed2006

The therapeutic potential of positive and negative immune cell co-stimulation during inflammation.

Inflammatory cascades are initiated in response to alarm signals that may result from infection, malignant transformation or trauma. Immunity, however, must be controlled; otherwise damage may occur to otherwise healthy tissue within the same microenvironment. Similarly, peripheral tolerance mechanisms must ensure that autoreactive thymic or bone marrow emigrants do not respond upon encounter with the autoantigen. Organized lymphoid structures such as lymph nodes, spleen and Peyer's patches appear to regulate inflammation successfully, displaying controlled expansion and contraction. However, when immune cells flood into effector sites, the organization of T- and B-lymphocytes is lacking. What controls inflammatory cascades in lymph nodes but rarely in effector sites is not clear. We believe the difference lies in the Toll-like receptor ligand load, which is high in effector sites and drives uncontrolled inflammation. Similarly, we believe that initiation of autoimmune inflammation is initiated by the liberation of inflammatory signals due to infection or trauma. In this review, we highlight some of the molecules responsible for maintaining an activated T-cell phenotype, strategies to interrupt these therapeutically and the impact of ligating inhibitory receptors on antigen-presenting cells.

Animals↗
PubMed2006

Programming, demarcating, and manipulating CD8+ T-cell memory.

In response to infection, antigen-specific CD8+ T cells undergo massive expansion in numbers, acquire effector mechanisms, and disseminate throughout the body. The expansion phase is followed by a contraction (death) phase, where 90-95% of antigen-specific CD8+ T cells are eliminated. The remaining antigen-specific CD8+ T cells form the initial memory pool, which can be stably maintained for life. In this review, we discuss evidence that early events after infection 'program' CD8+ T cells to expand, contract, and generate memory in a fashion that is largely insensitive to the duration of infection or antigen display. Recent data demonstrate, despite numerical stability, that memory CD8+ T-cell populations undergo phenotypic and functional changes with time after immunization. However, the early suggestion that specific markers can be used to identify memory CD8+ T cells has not been supported by recent studies. Thus, we argue that specific functional characteristics, such as the ability to persist and undergo vigorous secondary expansion leading to elevated memory cell numbers, remain the best markers of 'good' memory cells. Finally, we discuss experimental approaches to manipulate and accelerate generation of CD8+ T cells with memory characteristics, and how these systems can inform both basic and applied immunology.

Animals↗