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Results for “Immunologic Memory”

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At least 1,513 records · Page 84Linked to original sources
PubMed2003

B cells as effectors.

B cells act as immune effectors, primarily through antigen-specific clonal expansion and plasma-cell differentiation. B1 (CD5(+)) B cells and marginal zone B cells dominate T-cell independent humoral responses under the molecular control of activated dendritic cells. Helper T cell-regulated B-cell responses draw on follicular B cells as precursors and rely on qualitatively different patterns of immune synapse formation to regulate B-cell fate. These activities culminate in the germinal center reaction, during which somatic hypermutation and antigen-driven selection produce and preserve high-affinity plasma cells with extended longevity and memory B cells as the sensitized precursors for antigen recall.

Animals↗
PubMed1989

Memory T cells.

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Antigens, CD↗
PubMed2006

Why do B cells mutate their immunoglobulin receptors?

B cells have the unique ability to acquire large numbers of point mutations in the variable segment of rearranged immunoglobulin (Ig) genes during a germinal center reaction. It is broadly accepted that somatic hypermutation (SHM) and affinity maturation are required to generate memory B cells and to produce antibodies capable of accomplishing the host defense functions of the humoral component of the adaptive immune system. However, several studies illustrate that low-avidity interactions between antigen and the B-cell receptor can induce deletion, receptor editing and a T-dependent immune response, suggesting that the high-avidity binding of antigen is not essential. If enhanced antigen binding is not essential for immune responses, what is the purpose of SHM? An alternative benefit of SHM might be to enhance the ability of B cells to track antigens expressed by rapidly mutating microorganisms.

Antibodies↗
PubMed1980

Characteristics of transplantation immunity in the sponge, Callyspongia diffusa.

Very extensive polymorphism of histocompatibility (H) molecules in the sponge Callyspongia diffusa was revealed by the incompatibility found among 480 different allogeneic pairings without exception. This represents some 960 individual clones utilized as alloparabionts or sources of fitted allografts. Consistent cytotoxic reactivity provoked by allogeneic cell surface contact in Callyspongia is manifest in a continuum of strong to weak histoincompatibilities; however, strong reactions are most frequent at normal temperatures of 23 to 27 C. The directionality, vigor, and timing of alloparabiotic rejection in this species all depend mainly on the genetic constitutions of the interacting clones. Replicate interclonal combinations yield essentially identical rejection reactions, and differences in graft dosage had no effect on either the direction or intensity of allocytotoxicity. Alloreaction times are inversely proportional to the strength of the H barrier. Maximal allosensitization indicated by accelerated second-set reactivity was gradually achieved, as a function of the interclonal combination, after 2 to 8 days of primary contact. Heightened transplantation immunity or memory persists for at least 2 to 3 weeks after contact sensitization.

Animals↗
PubMed2006

Naïve and memory cell turnover as drivers of CCR5-to-CXCR4 tropism switch in human immunodeficiency virus type 1: implications for therapy.

Early human immunodeficiency virus infection is characterized by the predominance of CCR5-tropic (R5) virus. However, in many individuals CXCR4-tropic (X4) virus appears in late infection. The reasons for this phenotypic switch are unclear. The patterns of chemokine receptor expression suggest that X4 and R5 viruses have a preferential tropism for naïve and memory T cells, respectively. Since memory cells divide approximately 10 times as often as naïve cells in uninfected individuals, a tropism for memory cells in early infection may provide an advantage. However, with disease progression both naïve and memory cell division frequencies increase, and at low CD4 counts, the naïve cell division frequency approaches that of memory cells. This may provide a basis for the phenotypic switch from R5 to X4 virus observed in late infection. We show that a model of infection using observed values for cell turnover supports this mechanism. The phenotypic switch from R5 to X4 virus occurs at low CD4 counts and is accompanied by a rapid rise in viral load and drop in CD4 count. Thus, low CD4 counts are both a cause and an effect of X4 virus dominance. We also investigate the effects of different antiviral strategies. Surprisingly, these results suggest that both conventional antiretroviral regimens and CCR5 receptor-blocking drugs will promote R5 virus over X4 virus.

Anti-HIV Agents↗
PubMed2005

Persistence of viral infections on the population level explained by an immunoepidemiological model.

We consider a mathematical model of viral spread in a population based on an immune response model embedded in an epidemic network model. The immune response model includes virus load and effector and memory T cells with two possible outcomes depending on parameters: (a) virus clearance and establishment of immune memory and (b) establishment of a non-zero viral presence characterized with increased T-cell concentrations. Isolated individuals can have different immune system parameters and, after a primary infection, can either return to the infection-free state or develop persistent or chronic infection. When individuals are connected in the network, they can reinfect each other. We show that the virus can persist in the epidemic network for indefinite time even if the whole population consists of individuals that are able to clear the virus when isolated from the network. In this case a few individuals with a relatively weak immune response can maintain the infection in the whole population. These results are in contrast to implications of classical epidemiological models that a viral epidemic will end if there is no influx of new susceptibles and if individuals can become immune after infection.

Adenoviridae Infections↗
PubMed2002

Dissecting the complexity of the memory T cell response.

Memory immune responses are classically attributed to the reactivation of long-lived, antigen-specific T lymphocytes that persist in a quiescent state. Determining mechanisms for the generation of memory T cells and dissecting the functional nature of the memory T cell pool has been encumbered by an inability to distinguish recently activated effector T cells from memory T cells. We have established new activation and biochemical criteria that distinguish effector and memory T cells and have applied these criteria to follow memory generation from activated cells in vivo. We found that the resultant memory T cell pool is heterogeneous and consists of effector-like and resting memory-like subsets that differ in expression of the homing receptor, CD62L. We discuss these findings in the context of memory T cell heterogeneity identified in human and mouse systems. These results suggest that more than one type of previously activated T cell can mediate recall or memory immune responses and that elucidating the fundamental phenotypic and functional features of memory T cell subsets is therefore critical to deciphering the complex nature of the memory immune response.

Animals↗
PubMed2006

Pathogen responses to host immunity: the impact of time delays and memory on the evolution of virulence.

Current analytical models of the mammalian immune system typically assume a specialist predator-prey relationship between invading pathogens and the active components of the immune response. However, in reality, the specific immune system is not immediately effective following invasion by a novel pathogen. First, there may be an explicit time delay between infection and immune initiation and, second, there may be a gradual build-up in immune efficacy (for instance, during the period of B-cell affinity maturation) during which the immune response develops, before reaching maximal specificity to the pathogen. Here, we use a novel theoretical approach to show that these processes, together with the presence of long-lived immune memory, decouple the immune response from current pathogen levels, greatly changing the dynamics of the pathogen-immune system interaction and the ability of the immune response to eliminate the pathogen. Furthermore, we use this model to show how distributed primary immune responses combine with immune memory to greatly affect the optimal virulence of the pathogen, potentially resulting in the evolution of highly virulent pathogens.

Animals↗