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Results for “Immunologic Memory”

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At least 1,477 records · Page 82Linked to original sources
PubMed2003

Dynamical analysis of a degenerate primary and secondary humoral immune response.

Lymphocyte receptor response to antigen is degenerate. Each receptor can have a high affinity to more than one antigen. The optimal level of degeneracy was previously modeled using different methods; all showing that the degeneracy level should be inversely proportional to the probability that an antigen belongs to the self repertoire. Here we develop a new formalism, reproducing the results of previous models, which enables us to study the relation between receptor degeneracy and the pathogen-immune cell interaction dynamics, in primary and secondary response. We begin by developing a general formalism and reproducing the results obtained by Nemazee: (1) that an optimal immune system will have a capacity which is inversely proportional to the fraction of self-antigens and (2) that the number of self-reactive cells that the body destroys is tuned by this capacity optimization to be 63%. We then use our extended framework to relate the minimal number of B cell precursor required to mount an immune response to the naive B cell production rate. Finally, we analyze the dynamics of the interaction between the immune system and a pathogen and show that memory cells may be used as the first line of defense, while newly created cells are used later to refine the immune response.

Animals↗
PubMed1997

Modeling T-cell proliferation: an investigation of the consequences of the Hayflick limit.

Somatic cells, including immune cells such as T-cells have a limited capacity for proliferation and can only replicate for a finite number of generations (known as the Hayflick limit) before dying. In this paper we use mathematical models to investigate the consequences of introducing a Hayflick limit on the dynamics of T-cells stimulated with specific antigen. We show that while the Hayflick limit does not alter the dynamics of T-cell response to antigen over the short term, it may have a profound effect on the long-term immune response. In particular we show that over the long term the Hayflick limit may be important in determining whether an immune response can be maintained to a persistent antigen (or parasite). The eventual outcome is determined by the magnitude of the Hayflick limit, the extent to which antigen reduces the input of T-cells from the thymus, and the rate of antigen-induced proliferation of T-cells. Counter to what might be expected we show that the persistence of an immune response (immune memory) requires the density of persistent antigen to be less than a defined threshold value. If the amount of persistent antigen (or parasite) is greater than this threshold value then immune memory will be relatively short lived. The consequences of this threshold for persistent mycobacterial and HIV infections and for the generation of vaccines are discussed.

Antigens↗
PubMed1998

Models of immune memory: on the role of cross-reactive stimulation, competition, and homeostasis in maintaining immune memory.

There has been much debate on the contribution of processes such as the persistence of antigens, cross-reactive stimulation, homeostasis, competition between different lineages of lymphocytes, and the rate of cell turnover on the duration of immune memory and the maintenance of the immune repertoire. We use simple mathematical models to investigate the contributions of these various processes to the longevity of immune memory (defined as the rate of decline of the population of antigen-specific memory cells). The models we develop incorporate a large repertoire of immune cells, each lineage having distinct antigenic specificities, and describe the dynamics of the individual lineages and total population of cells. Our results suggest that, if homeostatic control regulates the total population of memory cells, then, for a wide range of parameters, immune memory will be long-lived in the absence of persistent antigen (T1/2 > 1 year). We also show that the longevity of memory in this situation will be insensitive to the relative rates of cross-reactive stimulation, the rate of turnover of immune cells, and the functional form of the term for the maintenance of homeostasis.

Animals↗
PubMed2002

T cell immunity in lymphoid and non-lymphoid tissues.

Immune responses to infection or effective vaccination generally result in the development of memory lymphocytes capable of mounting a rapid response to secondary infection. Since most infections initiate in non-lymphoid tissues, defense at these sites may be important for protection. Recent results suggest that a substantial portion of the T cell response to infection is focused in non-lymphoid tissues. Furthermore, anatomic localization appears to define phenotypic and functional heterogeneity among antigen-specific memory T cell populations.

Animals↗
PubMed1982

Immune characteristics of graft rejection in nemerteans of the genus Lineus.

The rejection of xenogeneic grafts in marine worms of the genus Lineus (Nemertea) gives evidence for the occurrence of immune mechanisms in these invertebrates. First, second-set response is anamnestic with a three-month memory component. Second, the accelerated rejection of second-set grafts occurs anywhere in the body of the recipient, that is to say it is systemic. Third, the anamnestic response is species-specific since it takes place only when second grafts are from donors of the same species as that of the first set. It is therefore plausible that the reaction to xenogeneic grafts is a cell-mediated immune mechanism and that the self-nonself discrimination may be a function of nemertean cells specialized for recognition at the species level and for memory.

Animals↗
PubMed2003

Cell-mediated immunity to respiratory virus infections.

The mucosal surfaces of the lungs pose tremendous problems for an immune system charged with maintaining a sterile pulmonary environment. Despite these problems, the immune system is effective at controlling most pulmonary infections. Over the past few years significant progress has been made in our understanding of how adaptive (humoral and cellular) immunity is able to control infections in the respiratory tract. Recent advances include the identification of effector memory T-cell populations in the lungs and an appreciation for the role of cytokines in regulating memory T-cell pools.

Humans↗
PubMed1996

Generation of T-cell memory.

Recent studies of T-cell memory have suggested that the persistent presence of the priming antigen is not necessary for maintenance of CD8 memory. Factors contributing to the development of memory from activated T cells remain ill defined but accumulating data suggest that cytokines play a key role in this process. There has also been recent progress in understanding turnover of naive and memory cells in the mouse.

Animals↗
PubMed1999

Reconciling repertoire shift with affinity maturation: the role of deleterious mutations.

The shift in Ab repertoire, from Abs dominating certain primary B cell responses to genetically unrelated Abs dominating subsequent "memory" responses, challenges the accepted paradigm of affinity maturation. We used mathematical modeling and computer simulations of the dynamics of B cell responses, hypermutation, selection, and memory cell formation to test hypotheses attempting to explain repertoire shift. We show that repertoire shift can be explained within the framework of the affinity maturation paradigm, only when we recognize the destructive nature of hypermutation: B cells with a high initial affinity for the Ag are less likely to improve through random mutations.

Antibody Affinity↗
PubMed2026

Transcriptome-Proteome Analysis of Human Naive and Memory B Cell Subsets Reveals Isotype and Subclass-Specific Phenotypes.

Antibodies produced by B cells aid in the recognition and clearance of pathogens and are the cornerstone of vaccination strategies. Humans produce nine different antibody isotypes, and their effector functions differ according to the type of antigen and route of exposure. Phenotypic variation between isotype-switched B cell subsets is expected but not studied in detail. To obtain a molecular definition of isotype-defined cell identity, we performed proteomics and transcriptomics on isotype-defined populations of human naive and memory B cells (MBCs): CD27-IgM+IgD+, CD27+CD38lo/-IgM+IgD+, CD27+CD38lo/-IgM+IgD-, and IgA1, IgA2, IgG1, IgG2, IgG3, and IgG4 MBCs (CD27+CD38lo/-Ig+). Combined proteome and transcriptome analysis revealed that mRNA and protein expression profiles separate isotype-defined B cell subsets according to their differentiation status. mRNA and protein expression levels correlated reasonably well for many genes. IgG4-switched B cells were most distinct from naive B cells in terms of mRNA as well as protein expression profiles. Besides a distinct expression profile of cytokine and Fc receptors, we identified a high expression of IgE-coding mRNA in IgG4-switched B cells. SDR16C5 was identified as uniquely upregulated in IgG4-switched B cells. Taken together, this study highlights the distinct phenotypic profile of IgG4-switched B cells.

Humans↗