PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Models, Immunological”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 505 records · Page 28Linked to original sources
PubMed2001

Stability of a diverse immunological memory is determined by T cell population dynamics.

The correlation between properties of the T cell memory pool and the two regulatory mechanisms of cell death (apoptosis) and memory entry (differentiation) is investigated mathematically. Apoptosis of T cells occurs at the end of an immune response, removing unwanted activated T cells. T cells escaping apoptosis enter the memory pool composed of T cells specific for previously encountered antigens. We find that the relative efficiencies of these two pathways determine the clonal distribution and the long-term stability of the memory pool by regulating the number of new entries. The main result presented in this paper is that immunological memory of previously encountered pathogens cannot be erased by either severe or repeat infections with a particular pathogen (the diversity of the memory pool is ensured) only if apoptosis and/or memory differentiation are regulated by population dependent processes. Furthermore, vaccination properties are improved significantly by population dependent mechanisms and our mathematical analysis reveals that the T cell population must communicate with other parts of the immune system to ensure optimal performance of immunological memory.

Apoptosis↗
PubMed1996

The analysis of limiting dilution assays conducted under non-saturating conditions.

A form of mathematical analysis is presented which permits an extended analysis of limiting dilution assays under conditions in which either accessory factors, or cells or both are limiting. This is in contrast to the traditional form of analysis which permits only a single limiting parameter. Both make use of in vitro experiments in order to determine the number of antibody-producing cell precursors: the traditional form of analysis requires that all accessory cells or their factors be present in saturating concentrations; whereas in the analytic method employed here, not only B cells, but also accessory cells (macrophages) or their factors may be limiting. Analysis under non-saturating conditions permits greater elucidation of the mechanisms of intercellular interaction.

Animals↗
PubMed2005

Mucosal effector memory T cells: the other side of the coin.

Immunological memory allows for rapid and effective protective immunity to previously encountered pathogens. New insights in understanding specific memory differentiation and function have now indicated that in addition to providing enhanced immunity, an important purpose of immunological memory is to provide immediate protection at all sites of the body, including non-lymphoid tissues. Effector memory CD8 T cells have the capacity to reside long-term at epithelial surfaces, where they allow for rapid containment of the invading pathogens at the local entry site and prevent systemic spreading and excessive immune responses. The accumulation of tissue-specific memory T cell subsets, together with cross-reactivity of these antigen-experienced T cells even to unrelated pathogens, provides flexibility and expansion of their specificity repertoire that over time greatly surpasses that of the declining naïve T cell populations. This review will discuss new insights into T cell memory. We will focus in particular on the generation and function of effector memory CD8 T cells at the intestinal mucosa, which represents one of the largest entry sites for pathogens.

Animals↗
PubMed2005

Innate-like B cells.

Numerous studies in several species have shown that certain subsets of T and B lymphocytes express antigen receptors which are either semi-invariant, or germline encoded, and often autoreactive. In the case of B cells they appear to use a distinct immune recognition strategy during developmental selection and functional activation. These B cells respond to foreign antigens, and have the ability to protect against a variety of infections; however, they can also react with self or neoself antigens. They appear to use the latter as positively selecting ligands facilitating their entry into and maintenance in a functional repertoire, as well as providing cues for positioning themselves in strategic microenvironmental niches in the immune system and at interfaces with the environment. These innate-like B cell subsets form a bridge between the rapidly occurring innate immune responses, and the slower acting primary, T cell-dependent, adaptive antibody response by providing a rapid T cell-independent antibody response.

Animals↗
PubMed1995

The cell biology of CTL killing.

A great deal is known about the immunology of cytotoxic T lymphocyte killing, but much less is known about the cell biology of this process. Recent work has begun to elucidate the mechanisms that control lytic-protein secretion, and reveals that some unusual features of these secretory processes might explain some of the important features of killing by cytotoxic T lymphocytes.

Apoptosis↗
PubMed2005

FoxP3: a genetic link between immunodeficiency and autoimmune diseases.

It has long been observed that patients with autoimmune diseases also have immune deficiency. How these two opposite extremes of immunity can be found in the same individual is largely unclear. Here we review the evidence that a FoxP3 defect may provide a critical link between autoimmunity and immune deficiency. Disruption of FoxP3 results in severe autoimmune syndromes in both human and mice. Bone marrow chimera experiments indicate that FoxP3 defects in both hematopoietic and non-hematopoietic cells are required for the development of severe autoimmune disease. FoxP3 mutation in the hematopoietic cells impairs the development of regulatory T cells (Treg). Our data demonstrate that the mutation in non-hematopoietic cells results in deficient thymopoiesis. Defective T cell production may be an underlying cause of T cell hyperproliferation, which together with Treg defects, may lead to fatal autoimmune disease in mouse and man.

Animals↗
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↗
PubMed2005

Effector lymphoid tissue and its crucial role in protective immunity.

It is often argued that T cell-mediated immunity to secondary infection is dependent on the 'accelerated' responses of memory T cells in lymph nodes. However, new evidence points to a crucial role for effector memory T cells, which are resident in peripheral tissues, in immune protection. These T cells, which reside in peripheral tissues, are not necessarily bound by an anatomical structure and can be present at many sites. Collectively, they represent a third functional tissue of the immune system, uniquely specialized to mediate protective immunity. We propose that the paradigm 'effector lymphoid tissue' needs to be articulated and developed as a focus of new research to describe and understand the unique role this tissue has in protective immunity.

Animals↗
PubMed2004

Dynamic optimization of host defense, immune memory, and post-infection pathogen levels in mammals.

When attacked by pathogens, higher vertebrates produce specific immune cells that fight against them. We here studied the host's optimal schedule of specific immune cell production. The damage caused by the pathogen increases with the pathogen amount in the host integrated over time. On the other hand, there is also a cost incurred by the production of specific immune cells, not only in terms of the energy needed to produce and maintain the cells, but also with respect to damages sustained by the host's body as a result of immune activity. The optimal strategy of the host is the one that minimizes the total cost, defined as a weighted sum of the damage caused by pathogens and the costs caused by the specific immune cells. The problem is solved by using Pontryagin's maximum principle and dynamic programming. The optimal defense schedule is typically as follows: In the initial phase after infection, immune cells are produced at the fastest possible rate. The amount of pathogen increases temporarily but is eventually suppressed. When the pathogen amount is suppressed to a sufficiently low level, the immune cell number decreases and converges to a low steady level, which is maintained by alternately switching between fastest production and no production. We examine the effect of time delay required to have fully active immune cells by comparing cases with different number of rate limiting steps before producing immune cells. We examine the effect of the duration of time (time delay) required before full-scale production of active immune cells by comparing cases with different numbers of rate-limiting steps before immune-cell production. We also discuss the role of immune memory based on the results of the optimal immune reaction.

Animals↗
PubMed2007

Apolipoprotein M likely extends its anti-atherogenesis via anti-inflammation.

Apolipoprotein M (apoM), a novel human apolipoprotein recently discovered, predominantly presents in high density lipoprotein (HDL) in plasma, exclusively expressed in liver and in kidney. The present data demonstrated apoM protects against atherosclerosis (AS) primarily via partaking in prebeta-HDL formation and promoting cholesterol efflux to HDL. However, this lipid-metabolism-associated pathway seems unlikely responsible for all atheroprotective effects of apoM. Notably, the human apoM gene is just located in the major histocompatibility complex class III region (MHC-III) on chromosome 6, many genes in this region are related to the immune and inflammatory response. Furthermore, apoM has been documented to link with some inflammatory factors including platelet activating factor (PAF) and leptin. These evidences indicate that apoM may be involved in inflammatory activities in vivo and the potential immuno- and inflam-reactive property of apoM may contribute to the anti-inflammatory function of HDL, as generally acknowledged as an important atheroprotective mechanism of HDL.

Apolipoproteins↗