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The cellular basis of T-cell memory.
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Exploring pathways for memory T cell generation.
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Antibody mediated suppression of the IgM memory.
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Recognition and memory in the cells of the immune system.
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The differentiation of cytotoxic T cells in vitro. III. The role of helper T cells and their products in the differentiation of cytotoxic cells from "memory" cell populations.
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No modulation of circulating natural killer cell and natural killer receptor bearing memory T cell subsets in patients with atopic dermatitis.
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Selection of anti-arsonate idiotype (CRIA) in A/J mice by the immune network.
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Selection in the mature B cell repertoire.
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SIV and HIV prophylaxis.
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Psoriasis: dysregulation of innate immunity.
The current understanding of the function of natural killer (NK) T cells in innate immunity and their potential to control acquired specific immunity, as well as the remarkable efficacy of antitumour necrosis factor-alpha biological treatments in psoriasis, forces us to refine the current T-cell hypothesis of psoriasis pathogenesis, and to give credit to the role of innate immunity. Psoriasis might be envisioned to be a genetically determined triggered state of otherwise dormant innate immunity. This aggravated state of innate immunity is represented by the activity of NK T cells, dendritic cells, neutrophils and keratinocytes, leading to the recruitment and activation of preferentially type 1 T cells, possibly in an antigen-independent way. Keratinocytes in psoriasis then are sensitive to the effects of T-cell activation and cytokine production, interferon (IFN)-gamma, by responding with psoriasiform hyperplasia. The chronic inflammation of psoriatic lesions suggests that this might be due to a deficiency in downregulation processes (e.g. a defect in the regulatory T-cell repertoire) and/or the persistence of an unknown trigger resulting in an exaggerated innate immune response.
[Relationship between the immunodepressant action of methotrexate and the dose of antigen].
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Physiology of IgD. VIII. Age-related decline in the capacity to generate T cells with receptors for IgD and partial reversal of the defect with IL 2.
In previous studies we have shown that T cells from young mice can be induced to express receptors for IgD (T delta cells) after in vivo or in vitro exposure to IgD or IL 2. In the present study, mice of three different strains were used to study the effects of aging on the ability of splenic T cells to express such receptors. It is shown that T cells from mice older than 18 mo of age are deficient with respect to their ability to express receptors for IgD after in vivo or in vitro exposure to IgD. Similarly, IFN-gamma induces T delta cells in young but not in aged mice. In contrast, T delta cells can be induced in aged mice with IL 2, although to a lower percentage than in young mice. In agreement with our previously reported findings, the current study demonstrates the immunoaugmenting effect of IgD injections on the antibody response in young mice. This effect is absent in aged mice and thus correlates with the failure of IgD to induce T delta cells in such animals.
Immunologic enhancement of normal tissue grafts.
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Allogeneic sensitization alters T-cell reactivity to extracellular matrix proteins in prospective transplant recipients.
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The challenge of inhibiting alloreactive T-cell memory.
Memory T cells specific for donor antigens present a unique challenge in transplantation. In addition to expressing rapid and robust immune responses to a transplanted organ, memory T cells may be resistant to the effects of currently used graft-prolonging therapies. The increasing recognition that alloreactive memory T cells participate in transplant rejection is driving new lines of research focusing on understanding the immunobiology of alloreactive memory T cells and on designing novel therapies to specifically target memory T cells. The purpose of this review is to summarize the effects of existing immunosuppressive drugs and costimulatory blockade on functions of alloreactive memory T cells that undermine allograft survival.
T cell memory.
Typical immune responses lead to prominent clonal expansion of antigen-specific T and B cells followed by differentiation into effector cells. Most effector cells die at the end of the immune response but some of these cells survive and form long-lived memory cells. The factors controlling the formation and survival of memory T cells are reviewed.