Immunity

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Rebecca M. Kilner - One of the best experts on this subject based on the ideXlab platform.

  • social Immunity of the family parental contributions to a public good modulated by brood size
    Evolutionary Ecology, 2016
    Co-Authors: Ana Duarte, Sheena C. Cotter, Catherine E Reavey, Richard J Ward, Ornela De Gasperin, Rebecca M. Kilner
    Abstract:

    Social Immunity refers to any immune defence that benefits others, besides the individual that mounts the response. Since contributions to social Immunity are known to be personally costly, they are contributions to a public good. However, individuals vary in their contributions to this public good and it is unclear why. Here we investigate whether they are responding to contributions made by others with experiments on burying beetle (Nicrophorus vespilloides) families. In this species, females, males and larvae each contribute to social Immunity through the application of antimicrobial exudates upon the carrion breeding resource. We show experimentally that mothers reduce their contributions to social Immunity when raising large broods, and test two contrasting hypotheses to explain why. Either mothers are treating social Immunity as a public good, investing less in social Immunity when their offspring collectively contribute more, or mothers are trading off investment in social Immunity with investment in parental care. Overall, our experiments yield no evidence to support the existence of a trade-off between social Immunity and other parental care traits: we found no evidence of a trade-off in terms of time allocated to each activity, nor did the relationship between social Immunity and brood size change with female condition. Instead, and consistent with predictions from models of public goods games, we found that higher quality mothers contributed more to social Immunity. Therefore our results suggest that mothers are playing a public goods game with their offspring to determine their personal contribution to the defence of the carrion breeding resource.

  • Personal Immunity versus social Immunity
    Behavioral Ecology, 2010
    Co-Authors: Sheena C. Cotter, Rebecca M. Kilner
    Abstract:

    It is well known that organisms defend their fitness against attack from parasites and pathogens by mounting a personal immune response. However, there is increasing evidence that organisms from diverse taxa also exhibit immune responses for the purpose of protecting other individuals as well as themselves. We argue that any type of Immunity that has fitness consequences for both the challenged individual and one or more recipients should be referred to as ‘social Immunity’. We show that social immune systems are a widespread yet relatively neglected component of Immunity, ideal for the study of social evolution. Whereas personal immune systems protect lifespan, social immune systems effectively defend the fecundity component of fitness, commonly protecting offspring or reproductive kin. We suggest that there are likely to be close links between life history and the extent of investment in each form of Immunity. Furthermore, trade-offs between social and personal Immunity may explain individual variation in personal immune responses, including sex-specific immune defences.

Sheena C. Cotter - One of the best experts on this subject based on the ideXlab platform.

  • social Immunity of the family parental contributions to a public good modulated by brood size
    Evolutionary Ecology, 2016
    Co-Authors: Ana Duarte, Sheena C. Cotter, Catherine E Reavey, Richard J Ward, Ornela De Gasperin, Rebecca M. Kilner
    Abstract:

    Social Immunity refers to any immune defence that benefits others, besides the individual that mounts the response. Since contributions to social Immunity are known to be personally costly, they are contributions to a public good. However, individuals vary in their contributions to this public good and it is unclear why. Here we investigate whether they are responding to contributions made by others with experiments on burying beetle (Nicrophorus vespilloides) families. In this species, females, males and larvae each contribute to social Immunity through the application of antimicrobial exudates upon the carrion breeding resource. We show experimentally that mothers reduce their contributions to social Immunity when raising large broods, and test two contrasting hypotheses to explain why. Either mothers are treating social Immunity as a public good, investing less in social Immunity when their offspring collectively contribute more, or mothers are trading off investment in social Immunity with investment in parental care. Overall, our experiments yield no evidence to support the existence of a trade-off between social Immunity and other parental care traits: we found no evidence of a trade-off in terms of time allocated to each activity, nor did the relationship between social Immunity and brood size change with female condition. Instead, and consistent with predictions from models of public goods games, we found that higher quality mothers contributed more to social Immunity. Therefore our results suggest that mothers are playing a public goods game with their offspring to determine their personal contribution to the defence of the carrion breeding resource.

  • Personal Immunity versus social Immunity
    Behavioral Ecology, 2010
    Co-Authors: Sheena C. Cotter, Rebecca M. Kilner
    Abstract:

    It is well known that organisms defend their fitness against attack from parasites and pathogens by mounting a personal immune response. However, there is increasing evidence that organisms from diverse taxa also exhibit immune responses for the purpose of protecting other individuals as well as themselves. We argue that any type of Immunity that has fitness consequences for both the challenged individual and one or more recipients should be referred to as ‘social Immunity’. We show that social immune systems are a widespread yet relatively neglected component of Immunity, ideal for the study of social evolution. Whereas personal immune systems protect lifespan, social immune systems effectively defend the fecundity component of fitness, commonly protecting offspring or reproductive kin. We suggest that there are likely to be close links between life history and the extent of investment in each form of Immunity. Furthermore, trade-offs between social and personal Immunity may explain individual variation in personal immune responses, including sex-specific immune defences.

Francois Meurens - One of the best experts on this subject based on the ideXlab platform.

  • humoral and cellular factors of maternal Immunity in swine
    Developmental and Comparative Immunology, 2009
    Co-Authors: H Salmon, Mustapha Berri, Volker Gerdts, Francois Meurens
    Abstract:

    Abstract Immunoglobulins cannot cross the placenta in pregnant sows. Neonatal pigs are therefore agammaglobulinemic at birth and, although immunocompetent, they cannot mount rapid immune responses at systemic and mucosal sites. Their survival depends directly on the acquisition of maternal Immunity via colostrum and milk. Protection by maternal Immunity is mediated by a number of factors, including specific systemic humoral Immunity, involving mostly maternal IgG transferred from blood to colostrum and typically absorbed within the first 36 h of life. Passive mucosal Immunity involves local humoral Immunity, including the production of secretory IgA (sIgA), which is transferred principally via milk until weaning. The mammary gland (MG) produces sIgA, which is, then secreted into the milk via the poly-Ig receptor (pIgR) of epithelial cells. These antibodies are produced in response to intestinal and respiratory antigens, including pathogens and commensal organisms. Protection is also mediated by cellular Immunity, which is transferred via maternal cells present in mammary secretions. The mechanisms underlying the various immunological links between MG and the mucosal surfaces involve hormonally regulated addressins and chemokines specific to these compartments. The enhancement of colostrogenic Immunity depends on the stimulation of systemic Immunity, whereas the enhancement of lactogenic Immunity depends on appropriate stimulation at induction sites, an increase in cell trafficking from the gut and upper respiratory tract to the MG and, possibly, enhanced immunoglobulin production at the effector site and secretion in milk. In addition, mammary secretions provide factors other than immunoglobulins that protect the neonate and regulate the development of mucosal Immunity—a key element of postnatal adaptation to environmental antigens.

  • Humoral and cellular factors of maternal Immunity in swine
    Developmental and Comparative Immunology, 2009
    Co-Authors: H Salmon, Mustapha Berri, Volker Gerdts, Francois Meurens
    Abstract:

    Immunoglobulins cannot cross the placenta in pregnant sows. Neonatal pigs are therefore agammaglobulinemic at birth and, although immunocompetent, they cannot mount rapid immune responses at systemic and mucosal sites. Their survival depends directly on the acquisition of maternal Immunity via colostrum and milk. Protection by maternal Immunity is mediated by a number of factors, including specific systemic humoral Immunity, involving mostly maternal IgG transferred from blood to colostrum and typically absorbed within the first 36 h of life. Passive mucosal Immunity involves local humoral Immunity, including the production of secretary IgA (slgA), which is transferred principally via milk until weaning. The mammary gland (MG) produces sIgA, which is, then secreted into the milk via the poly-Ig receptor (pIgR) of epithelial cells. These antibodies are produced in response to intestinal and respiratory antigens, including pathogens and commensal organisms. Protection is also mediated by cellular Immunity, which is transferred via maternal cells present in mammary secretions. The mechanisms underlying the various immunological links between MG and the mucosal surfaces involve hormonally regulated addressins and chemokines specific to these compartments. The enhancement of colostrogenic Immunity depends on the stimulation of systemic Immunity, whereas the enhancement of lactogenic Immunity depends on appropriate stimulation at induction sites, an increase in cell trafficking from the gut and upper respiratory tract to the MG and, possibly, enhanced immunoglobulin production at the effector site and secretion in milk. In addition, mammary secretions provide factors other than immunoglobulins that protect the neonate and regulate the development of mucosal Immunity-a key element of postnatal adaptation to environmental antigens. (c) 2008 Elsevier Ltd. All rights reserved.

Suzanne C. Segerstrom - One of the best experts on this subject based on the ideXlab platform.

  • Resources, Stress, and Immunity: An Ecological Perspective on Human Psychoneuroimmunology
    Annals of Behavioral Medicine, 2010
    Co-Authors: Suzanne C. Segerstrom
    Abstract:

    Ecological immunology provides a broad theoretical perspective on phenotypic plasticity in Immunity, that is, changes related to the value of Immunity across different situations, including stressful situations. Costs of a maximally efficient immune response may at times outweigh benefits, and some aspects of Immunity may be adaptively suppressed. This review provides a basic overview of the tenets of ecological immunology and the energetic costs of Immunity and relates them to the literature on stress and Immunity. Sickness behavior preserves energy for use by the immune system, acute stress mobilizes “first-line” immune defenders while suppressing more costly responses, and chronic stress may suppress costly responses in order to conserve energy to counteract the resource loss associated with stress. Unexpected relationships between stress “buffers” and immune functions demonstrate phenotypic plasticity related to resource pursuit or preservation. In conclusion, ecological models may aid in understanding the relationship between stress and Immunity.

Mihai G. Netea - One of the best experts on this subject based on the ideXlab platform.

  • Trained Immunity: A program of innate immune memory in health and disease
    Science, 2016
    Co-Authors: Mihai G. Netea, Leo A. B. Joosten, Eicke Latz, Kingston H. G. Mills, Gioacchino Natoli, Hendrik G. Stunnenberg, Luke A. J. O'neill, Ramnik J. Xavier
    Abstract:

    The general view that only adaptive Immunity can build immunological memory has recently been challenged. In organisms lacking adaptive Immunity, as well as in mammals, the innate immune system can mount resistance to reinfection, a phenomenon termed "trained Immunity" or "innate immune memory." Trained Immunity is orchestrated by epigenetic reprogramming, broadly defined as sustained changes in gene expression and cell physiology that do not involve permanent genetic changes such as mutations and recombination, which are essential for adaptive Immunity. The discovery of trained Immunity may open the door for novel vaccine approaches, new therapeutic strategies for the treatment of immune deficiency states, and modulation of exaggerated inflammation in autoinflammatory diseases.

  • training innate Immunity the changing concept of immunological memory in innate host defence
    European Journal of Clinical Investigation, 2013
    Co-Authors: Mihai G. Netea
    Abstract:

    The inability of innate Immunity to build an immunological memory is considered a main difference with adaptive Immunity. This concept has been challenged by studies in plants, invertebrates and mammals. Recently, a paradigm shift in our understanding host defence has been triggered by the mounting evidence for innate immune memory, leading to increased responses to secondary infections. Important differences between the cell populations and the molecular mechanisms exist between the adaptive traits of innate host defence on the one hand and immunological memory of adaptive Immunity on the other hand. The lasting state of enhanced innate Immunity termed ‘trained Immunity’ is mediated by prototypical innate immune cells such as natural killer cells and monocytes/macrophages. It provides protection against reinfection in a T/B-cell-independent manner, with both specific mechanisms and nonspecific epigenetic reprogramming mediating these effects. This concept represents a paradigm change in Immunity, and its putative role in resistance to reinfection may represent the next step in the design of future vaccines.