Immune response complex

A cascade of proteins of the immune response that can be triggered by antigen-antibody complexes and by the innate immune system (e.g. exposure to microbial polysaccharides) to raise the immune response. Complement proteins can detect and bind to foreign material or immune complexes and label them for phagocytosis. They can also cause inflammation by directly degranulating mast cells and releasing chemokines to recruit other immune cells into the affected area. 

Cell-mediated immunity (CMI) is the result of the activity of many leukocyte actions, reactions, and interactions that range from simple to complex. This type of immunity is dependent on the actions of the T lymphocytes, which are responsible for a delayed type of immune response The T lymphocyte becomes sensitized... 

Cyanidin is the most common anthocyanin in foods. In addition, anthocyanins are stabilized by the formation of complexes with other flavonoids (co-pigmentation). In the United States, the daily anthocyanin consumption is estimated at about 200 mg. Several promising studies have reported that consumption of anthocyanin-rich foods is associated with reductions of the risks of cancers - and atherosclerosis and with preventive effects against age-related neuronal and behavioral declines. These beneficial effects of anthocyanins might be related to their reported biological actions such as modulators of immune response and as antioxidants. Knowledge of anthocyanin bioavailability and metabolism is thus essential to better understand their positive health effects. 

Psoriasis is a T-lymphocyte-mediated inflammatory disease that results from a complex interplay between multiple genetic factors and environmental influences. Genetic predisposition coupled with some precipitating factor triggers an abnormal immune response, resulting in the initial psoriatic skin lesions. Keratinocyte proliferation is central to the clinical presentation of psoriasis. 

Taken as a whole, these observations show that parasite lines differ in an immune-dependent manner in their infection/expulsion kinetics. Furthermore, there is heritable variation in survival and fecundity in previously exposed hosts and quantitative variation in the immune response that selected parasite lines elicit. Again, taken as a whole, these observations have the necessary corollary that variation in these traits exists not only in laboratory-maintained isolates but also in helminth species in nature. The phenotypes under consideration here (infection/expulsion kinetics, survival, fecundity) are multifactorial life-history traits. Understanding the basis of variation in the components and interplay of these complex, immune-responsive phenotypes must be of crucial relevance to understanding the immunology of infections of parasitic nematodes. This is of particular relevance in view of current attempts to develop immunological methods of nematode control. 

Other contributions to this book have taken a molecular view of parasitic nematodes, yet molecules make only a rather brief appearance here. This chapter has tried to show that parasitic nematodes are fascinatingly and tantalizingly diverse at a phenotypic level. It has focused particularly on diversity in phenotypes that are apparent in response to environmental conditions within or outside a host. The interaction of parasites with within-host factors is a major current research effort. However, helminth immunology is particularly notable for its inattention to diversity, especially when compared with the immunology of parasitic protozoa (Read and Viney, 1996). Observations of the interaction of host immunity with subsequent development in S. ratti show the potential power of such interactions. It is also clear that a principal mechanism of the action of host immune responses is against nematode fecundity (Stear et al., 1997). This is likely to be a molecularly complex interaction. Understanding this interaction, as well as variation in the interaction is interesting, but could also form the basis of control by transmission-reduction rather than eradication per se. 

Studies with a variety of genetically modified mice have shed new light on the complex relationship between the protective and pathological immune responses controlling parasite infections. TNF and NO are important components of the pathological response accompanying the expulsion of a gastrointestinal nematode parasite. In the absence of TNF-R1 or iNOS, mice do not develop the severe villus atrophy and mucosal mastocytosis that usually accompany infection with T. spiralis, but their ability to expel the... 

Homo sapiens (compared to Drosophila melanogaster) Large-scale gene duplications with substantial expansion of genes involved in acquired immune response (B cells, T cells, major histocompatibility complex genes, cytokines, chemokines and their receptors), plasma proteases (complement and hemostatic proteins), proteins associated with apoptotic regulation and proteins related to neuronal network formation and electrical coupling... 

Microbial virulence is often the outcome of the complex interactions that take place as the pathogen establishes itself in the human host. The molecular determinants of pathogenicity include factors that cause damage to the host cell and those that help the microbe establish productive infection for survival [35]. The human host immune response counters the presence of these microbes with its acquired or innate immune response arsenal with outcomes that range from acute to chronic or latent infections. A clear definition of the host and microbial... 

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