Eosinophilia immune response

Halothane reduces splanchnic and hepatic blood flow. Halothane can produce fulminant hepatic necrosis in a small number of patients, a syndrome characterized by fever, anorexia, nausea, and vomiting, developing several days after anesthesia and sometimes accompanied by a rash and peripheral eosinophilia. There is a rapid progression to hepatic failure, with a fatality rate of -50%. This syndrome occurs in about 1 in 10,000 patients receiving halothane and is referred to as halothane hepatitis. Halothane hepatitis may be the result of an immune response to hepatic proteins that become trifluoroacetylated as a consequence of halothane metabolism see Pharmacokinetics, above). 

Egg-induced immunity appears to involve stage-specific immunogens against (a) the tissue phase of egg challenge (early response) and (b) the lumen phase of cysticercoid challenge (late response). This immunogenetic pattern is thus similar to the development of early and late immunity in larval taeniid cestodes (Fig. 11.7). The effector mechanism of the early response has been shown to be thymus dependent, X-irradiation sensitive, cell mediated and antibody mediated the response is visualised by eosinophilia infiltration around the invading oncospheres (Fig. 11.6) (353). 

T cells are the principal source of IgE regulatory cytokines. CD4 T cells can be subdivided on the basis of the cytokines they secrete. These subsets have been termed T helper 1 (ThI) and T helper 2 (Th2) (Mos-mann etal., 1986 Mosmann, 1992) on the basis of the cytokines that they produce. ThI cells make IFN7, IL-2 and TNF 8 and effect cell-mediated immunity. In the mouse, ThI cells support IgG2a antibody production. Th2 cells make IL-4, IL-5, IL-6 and II IO, support IgE responses and cause eosinophilia. Some cytokines, e.g. IL-3, TNFa and granulocyte-macrophage colony stimulating fector (GM-CSF), are secreted in similar amounts by both subsets (Table 3.2). In addition to ThI and Th2 cells there are other subtypes such as ThO, which exhibit an unrestricted cytokine profile (Firestein et al., 1989), and there are probably others, such as a non-cytolytic vesicular stomatitis virus-specific 004" T cell clone which produces IL-6, TNFa and TNF/3 but not IL-2, IL-4 or IFN7 (Gao et al., 1993). 

Emslie-Smith AM, Engel A, Duffy J, Bowles CA (1991) Eosinophilia myalgia syndrome I. Immunocytochemical evidence for a T-cell mediated immune effector response. Ann Neurol, 29 524-528. 

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