Adaptive Memory Summary

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Adaptive Memory Summary



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Seel Ed. New York, NY: Springer. Adaptive memory: Nature's criterion and the functionalist agenda. The American Journal of Psychology, 4 , Memory functions. Adaptive Memory: Evolutionary constraints on remembering. Ross Ed. Burlington: Academic Press. Adaptive memory: Remembering with a stone-age brain. Current Directions in Psychological Science, 17 4 , The functionalist agenda in memory research.

Healy Ed. Fernandes, S. The mnemonic tuning for contamination: A replication and extension study using more ecologically-valid stimuli. Evolutionary Psychology. Animacy norms for european portuguese concrete words. Fernandes, N. Presenting new stimuli to study emotion: Development and validation of the objects-on-hands picture database. Adaptive memory: longevity and learning intentionality of the animacy effect.

Journal of Cognitive Psychology. DOI: Adaptive memory: The mnemonic power of survival-based generation. Coverdale, M. Survival processing in a novel choice procedure. The American Journal of Psychology. Pandeirada, J. Adaptive memory: Remembering potential mates. Evolutionary Psychology , 15 4 , Adaptive memory: Temporal, semantic, and rating-based clustering following survival processing. Journal of Memory and Language , 93, Adaptive memory: The mnemonic value of contamination.

Evolution and Human Behavior , in press. VanArsdall, J. A categorical recall strategy does not explain animacy effects in episodic memory. The Quarterly Journal of Experimental Psychology. Advance online publication. Source-constrained retrieval and survival processing. Adaptive memory: Animacy effects persist in paired-associate learning. Memory 23 5 , Adaptive memory: The mnemonic value of animacy. Psychological Science , 24 10 , Adaptive memory: Animacy processing produces mnemonic advantages. Adaptive memory: Enhanced location memory after survival processing. Congruity effects in the survival processing paradigm. Adaptive memory: Ancestral priorities and the mnemonic value of survival processing. Cognitive Psychology, 61 1 , Adaptive memory: Fitness-relevance and the hunter-gatherer mind.

Psychological Science, 20 6 , Adaptive memory: Is survival processing special? Journal of Memory and Language, 59 3 , Adaptive memory: The comparative value of survival processing. Psychological Science, 19 2 , Adaptive memory: Survival processing enhances retention. November, The mnemonic effect of choice. Poster presented at the 59th Annual Meeting of the Psychonomic Society. New Orleans, LA. The functionalist agenda in memory research Invited keynote speaker.

Liverpool, UK. August, Liverpool, United Kingdom. May, Adaptive memory: Exploring survival processing in a new choice procedure. San Francisco, CA. April, The Objects-on-Hands Picture database: Development and validation. Braga, Portugal. Machluf, K. Development of the animacy memory effect: 2nd and 5th graders replicate adult performance. Paper presented at the 58th Annual Meeting of the Psychonomic Society. Vancouver, BC. Adaptive memory: Evidence from alternative procedures. Meeting of the Society of Experimental Psychologists. Nashville, TN. Adaptive memory for dummies. The factors that dictate whether an infection triggers a Th1 or Th2 type response are not fully understood, but the response generated does play an important role in the clearance of different pathogens.

The Th1 response is characterized by the production of Interferon-gamma , which activates the bactericidal activities of macrophages, and induces B cells to make opsonizing marking for phagocytosis and complement-fixing antibodies, and leads to cell-mediated immunity. The Th2 response is characterized by the release of Interleukin 5 , which induces eosinophils in the clearance of parasites. Tfh cells are specialized in helping B cell humoral immunity as they are uniquely capable of migrating to follicular B cells in secondary lymphoid organs and provide them positive paracrine signals to enable the generation and recall production of high-quality affinity-matured antibodies.

Similar to Tregs, Tfh cells also play a role in immunological tolerance as an abnormal expansion of Tfh cell numbers can lead to unrestricted autoreactive antibody production causing severe systemic autoimmune disorders. On the other hand, however, the various subsets may also be considered part of the innate immune system where a restricted TCR or NK receptors may be used as a pattern recognition receptor.

B Cells are the major cells involved in the creation of antibodies that circulate in blood plasma and lymph, known as humoral immunity. Antibodies also known as immunoglobulin, Ig , are large Y-shaped proteins used by the immune system to identify and neutralize foreign objects. Upon activation, B cells produce antibodies, each of which recognize a unique antigen, and neutralizing specific pathogens. All the BCR of any one clone of B cells recognizes and binds to only one particular antigen. A critical difference between B cells and T cells is how each cell "sees" an antigen.

T cells recognize their cognate antigen in a processed form — as a peptide in the context of an MHC molecule, [2] whereas B cells recognize antigens in their native form. Plasma cells are short-lived cells 2—3 days that secrete antibodies. These antibodies bind to antigens, making them easier targets for phagocytes, and trigger the complement cascade. These molecules are believed to bind pathogenic antigens in a similar way to antibodies, and with the same degree of specificity.

For a long time it was thought that insects and other invertebrates possess only innate immune system. However, in recent years some of the basic hallmarks of adaptive immunity have been discovered in insects. Those traits are immune memory and specificity. Although the hallmarks are present the mechanisms are different from those in vertebrates. Immune memory in insects was discovered through the phenomenon of priming. When insects are exposed to non-lethal dose or heat killed bacteria they are able to develop a memory of that infection that allows them to withstand otherwise lethal dose of the same bacteria they were exposed to before. Instead those mechanisms are mediated by hemocytes. Hemocytes function similarly to phagocytes and after priming they are able to more effectively recognize and engulf the pathogen.

For example, in honeybees if the queen is infected with bacteria then the newly born workers have enhanced abilities in fighting with the same bacteria. Most commonly accepted theory of the specificity is based on Dscam gene. Dscam gene also known as Down syndrome cell adhesive molecule is a gene that contains 3 variable Ig domains. Those domains can be alternatively spliced reaching high numbers of variations. After the animals with different splice forms are exposed to the same pathogen only the individuals with the splice form specific for that pathogen survive. RNAi is a form of antiviral immunity with high specificity. When B cells and T cells are activated some become memory B cells and some memory T cells. Throughout the lifetime of an animal these memory cells form a database of effective B and T lymphocytes.

Upon interaction with a previously encountered antigen, the appropriate memory cells are selected and activated. In this manner, the second and subsequent exposures to an antigen produce a stronger and faster immune response. This is "adaptive" in the sense that the body's immune system prepares itself for future challenges, but is "maladaptive" of course if the receptors are autoimmune. Immunological memory can be in the form of either passive short-term memory or active long-term memory. Passive memory is usually short-term, lasting between a few days and several months. Newborn infants have had no prior exposure to microbes and are particularly vulnerable to infection. Several layers of passive protection are provided by the mother.

In utero , maternal IgG is transported directly across the placenta , so that, at birth, human babies have high levels of antibodies, with the same range of antigen specificities as their mother. This is passive immunity because the fetus does not actually make any memory cells or antibodies: It only borrows them. Short-term passive immunity can also be transferred artificially from one individual to another via antibody-rich serum. In general, active immunity is long-term and can be acquired by infection followed by B cell and T cell activation, or artificially acquired by vaccines, in a process called immunization. Historically, infectious disease has been the leading cause of death in the human population. Over the last century, two important factors have been developed to combat their spread: sanitation and immunization.

The principle behind immunization is to introduce an antigen, derived from a disease-causing organism, that stimulates the immune system to develop protective immunity against that organism, but that does not itself cause the pathogenic effects of that organism. An antigen short for anti body gen erator , is defined as any substance that binds to a specific antibody and elicits an adaptive immune response. Most viral vaccines are based on live attenuated viruses, whereas many bacterial vaccines are based on acellular components of microorganisms, including harmless toxin components.

Most large molecules, including virtually all proteins and many polysaccharides , can serve as antigens. Most antigens contain a variety of epitopes and can stimulate the production of antibodies, specific T cell responses, or both. For the acquired response to "remember" and eliminate a large number of pathogens the immune system must be able to distinguish between many different antigens, [1] and the receptors that recognize antigens must be produced in a huge variety of configurations, in essence one receptor at least for each different pathogen that might ever be encountered.

Even in the absence of antigen stimulation, a human can produce more than 1 trillion different antibody molecules. Myriad receptors are produced through a process known as clonal selection. To generate each unique antigen receptor, these genes have undergone a process called V D J recombination , or combinatorial diversification , in which one gene segment recombines with other gene segments to form a single unique gene. This assembly process generates the enormous diversity of receptors and antibodies, before the body ever encounters antigens, and enables the immune system to respond to an almost unlimited diversity of antigens.

Note that the innate and acquired portions of the immune system work together, not in spite of each other. The acquired arm, B, and T cells couldn't function without the innate system input. T cells are useless without antigen-presenting cells to activate them, and B cells are crippled without T cell help. On the other hand, the innate system would likely be overrun with pathogens without the specialized action of the adaptive immune response. The cornerstone of the immune system is the recognition of "self" versus "non-self".

Therefore, the mechanisms that protect the human fetus which is considered "non-self" from attack by the immune system, are particularly interesting. Although no comprehensive explanation has emerged to explain this mysterious, and often repeated, lack of rejection, two classical reasons may explain how the fetus is tolerated. The first is that the fetus occupies a portion of the body protected by a non-immunological barrier, the uterus , which the immune system does not routinely patrol.

During pregnancy in viviparous mammals all mammals except Monotremes , endogenous retroviruses ERVs are activated and produced in high quantities during the implantation of the embryo. They are currently known to possess immunosuppressive properties, suggesting a role in protecting the embryo from its mother's immune system. Also, viral fusion proteins cause the formation of the placental syncytium [23] to limit exchange of migratory cells between the developing embryo and the body of the mother something an epithelium can't do sufficiently, as certain blood cells specialize to insert themselves between adjacent epithelial cells.

The immunodepressive action was the initial normal behavior of the virus, similar to HIV. The fusion proteins were a way to spread the infection to other cells by simply merging them with the infected one HIV does this too. It is believed that the ancestors of modern viviparous mammals evolved after an infection by this virus, enabling the fetus to survive the immune system of the mother.

The human genome project found several thousand ERVs classified into 24 families. A theoretical framework explaining the workings of the acquired immune system is provided by immune network theory , based on interactions between idiotypes unique molecular features of one clonotype, i. This theory, which builds on the existing clonal selection hypothesis and since has been developed mainly by Niels Jerne and Geoffrey W. One of the most interesting developments in biomedical science during the past few decades has been elucidation of mechanisms mediating innate immunity. One set of innate immune mechanisms is humoral, such as complement activation. Another set comprises pattern recognition receptors such as toll-like receptors , which induce the production of interferons and other cytokines increasing resistance of cells such as monocytes to infections.

Unstable HbS clusters Band-3, a major integral red cell protein; [27] antibodies recognize these clusters and accelerate their removal by phagocytic cells. Clustered Band 3 proteins with attached antibodies activate complement, and complement C3 fragments are opsonins recognized by the CR1 complement receptor on phagocytic cells. A population study has shown that the protective effect of the sickle-cell trait against falciparum malaria involves the augmentation of acquired as well as innate immune responses to the malaria parasite, illustrating the expected transition from innate to acquired immunity.

Repeated malaria infections strengthen acquired immunity and broaden its effects against parasites expressing different surface antigens. By school age most children have developed efficacious adaptive immunity against malaria. These observations raise questions about mechanisms that favor the survival of most children in Africa while allowing some to develop potentially lethal infections. In malaria, as in other infections, [26] innate immune responses lead into, and stimulate, adaptive immune responses. The genetic control of innate and acquired immunity is now a large and flourishing discipline. Humoral and cell-mediated immune responses limit malaria parasite multiplication, and many cytokines contribute to the pathogenesis of malaria as well as to the resolution of infections.

The acquired immune system, which has been best-studied in mammals, originated in jawed fish approximately million years ago. Most of the molecules, cells, tissues, and associated mechanisms of this system of defense are found in cartilaginous fishes. The most ancient Ig class, IgM, is membrane-bound and then secreted upon stimulation of cartilaginous fish B cells. Another isotype, shark IgW, is related to mammalian IgD. The organization of gene segments that undergo gene rearrangement differs in cartilaginous fishes, which have a cluster form as compared to the translocon form in bony fish to mammals. Genes involved in antigen processing and presentation , as well as the class I and class II genes, are closely linked within the MHC of almost all studied species.

Lymphoid cells can be identified in some pre-vertebrate deuterostomes i. In jawless fishes , two subsets of lymphocytes use variable lymphocyte receptors VLRs for antigen binding. Yet, a comparative approach finds that many features are quite uniform across taxa. All the major features of the AIS arose early and quickly. Jawless fishes have a different AIS that relies on gene rearrangement to generate diverse immune receptors with a functional dichotomy that parallels Ig and TCR molecules.

Immunity can be acquired either actively or passively. Immunity is acquired actively when a person is exposed to foreign substances and the immune system responds. Passive immunity is when antibodies are transferred from one host to another. Both actively acquired and passively acquired immunity can be obtained by natural or artificial means. From Wikipedia, the free encyclopedia. Subsystem of the immune system that is composed of specialized, systemic cells and processes.

This article is about human immunity. For the same concept in botany, see Plant-induced systemic resistance. Main article: Lymphocyte. Main article: Antigen presentation. Main article: T cell. Main article: Cytotoxic T cell. Main article: T helper cell. Main article: Gamma delta T cell. Main articles: B cell and Humoral immunity. Main article: Adaptive immunity in jawless vertebrates. Further information: Immunity medical. Main article: Immune network theory.

Affinity maturation Allelic exclusion Anergy Immune response Immune tolerance Immunosuppression Original antigenic sin Somatic hypermutation Polyclonal response. Molecular Biology of the Cell 4th ed. New York and London: Garland Science. ISBN Immunobiology 5th ed. University of South Carolina School of Medicine. Archived from the original on 2 September

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