Host immune responses

Immunological reactions of the host to either the delivery vehicle or its cargo are another concern. The host immune response might not only eliminate the vector... 

Manno CS, Pierce GF, Arrada VR et al (2006) Successful transduction of liver in hemophilia by AAV-Factor IX and limitations imposed by the host immune response. Nat Med 12(3) 342-347... 

A number of chimerized, humanized, and one human mAb have now been approved for therapeutic use in humans in the treatment of autoimmunity, malignancy, infection and cardiovascular disease (Table 1). Some of the currently licensed mAb will be discussed here. A much larger number of mAb are currently being evaluated in Phase I, II and III trials. In general, chimeric, humanized and human mAb are very well tolerated with few side effects. Chimeric or humanized mAb still have the potential to evoke host immune response to the variable domains or CDRs of the antibody so-called HACA (human anti-chimeric antibody) or HAHA (human anti-human antibody) responses, although these responses are uncommon. Short-lived and occasionally severe infusion-related acute hypersensitivity reactions such as fever, skin itching, shivering, respiratory compromise and low blood pressure sometimes occur-. Such effects may... 

Hoschele D (2006) Cell culture models for the investigation of NRTI-induced mitochondrial toxicity. Relevance for the prediction of clinical toxicity. Toxicol In Vitro 20(5) 535-546 Itescu S, Brancato LJ et al (1989) A sicca syndrome in HIV infection association with HLA-DR5 and CDS lymphocytosis. Lancet 2(8661) 466 68 Itescu S, Brancato LJ et al (1990) A diffuse infiltrative CDS lymphocytosis syndrome in human immunodeficiency virus (HIV) infection a host immune response associated with HLA-DR5. Ann Intern Med 112(1) 3-10... 

Multiple factors play a role in the development of AOM. Viral infection of the nasopharynx impairs eustachian tube function and causes mucosal inflammation, impairing mucociliary clearance and promoting bacterial proliferation and infection. Children are predisposed to AOM because their eustachian tubes are shorter, more flaccid, and more horizontal than adults, which make them less functional for drainage and protection of the middle ear from bacterial entry. Clinical signs and symptoms of AOM are the result of host immune response and damage to cells caused by inflammatory mediators such as tumor necrosis factor and interleukins that are released from bacteria.4... 

For much of its life cycle a parasite s environment is its host. A principal, and potentially lethal, feature of this environment is the host immune response. Diversity in parasites interactions with this aspect of their environment may therefore be expected. The host immune response varies between different hosts and so, if this is considered as a selection pressure, it may produce the ideal conditions for the generation of diversity in immune-mediated parasite-host interactions. 

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. 

Bolas-Fernandez, F. and Wakelin, D. (1989) Infectivity of Trichinella isolates in mice is determined by host immune responsiveness. Parasitology 99, 83-88. 

Host and parasite have coevolved over millions of years and exist in mutual tolerance, disease only being apparent when the balance is upset by the host being exposed to unusually high parasite burdens at times when immunocompetence is diminished by age, physiological state, disease or nutritional status. The host immune response is multifaceted and it is... 

DNA viruses modulate the host immune response, e.g., most likely the etiologic agent of Kaposfs sarcoma, KSHV (human herpes vims —8), has captured complement-binding proteins, three cytokines (two macrophage inflammatory proteins and interleukin 6), bcl-2, interferon regulatory factors, interleukin 8 receptor. Certain retroviruses... 

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... 

Mohan, V.P. et al., Effects of tumor necrosis factor alpha on host immune response in chronic persistent tuberculosis Possible role for limiting pathology, Infect. Immun., 69, 1847, 2001. 

This chapter presents specific information with regard to the effects of environmental and occupational exposure to arsenic on inflammatory processes, the immune system, and host defense. While the focus is on the in vivo and in vitro effects of arsenic on host immune responses (e.g., immunotoxicity and hypersensitivity) and their relationship to clinically observed manifestations of arsenic toxicity (e.g., inflammation and skin cancer), information on the potential mechanisms through which arsenic may exert its biological effects is also provided. 

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