Eosinophil Effector Mechanisms

Cytokines and chemokines made by cells such as keratinocytes, macrophages and LC might be expected to recruit and activate leukocytes, which have the potential to kill schistosomula before the development of any adaptive immunity. In vitro, schistosomula have been shown to be susceptible to a wide array of immune effector mechanisms mediated by eosinophils and neutrophils (Butterworth, 1984 Capron and Capron,... 

Thus, for the Hymenolepidids the data can be interpreted to fit the Th2 paradigm with the involvement of the predicted immune/ physiological effector mechanisms AB, complement, mast cells, eosinophils and goblet cells. 

Effector mechanism Mast cell and basophil activation Complement fixation Phagocytes, NK cells (Fc receptor cells) Complement Hiagocytes Macrophage activation Cytotoxic lymphocytes Eosinophil activation... 

Bronchial Asthma. Figure 2 Mechanisms of bronchial hyperresponsiveness. Toxic products from eosinophils [cationic peptides, reactive oxygen species (ROS)] cause epithelial injury. Nerve endings become easily accessible to mediators from mast cells, eosinophils [eosinophil-derived neurotoxin (EDN)], and neutrophils, and to airborne toxicants such as S02. Activation of nerve endings stimulates effector cells like mucosal glands and airway smooth muscle either directly or by cholinergic reflexes. 

Eosinophilia is a hallmark of intestinal nematode infection and is known to be under the control of IL-5 (Finkelman et al., 1992). As discussed above, treatment with anti-IL-5 monoclonal antibody (and so ablation of eosinophilia) had no effect on expulsion of T. muris, 77. polygyms, N. brasiliensis or T. spiralis infections, suggesting that either redundant mechanisms operate under these circumstances or that eosinophils are not a critical component of effector responses operating against most murine... 

The progression of airway inflammations involves several types of cells such as CD4", Th2 cells, eosinophils, and mast cells (Wills-Karp, 1999). The immunopathogenic role of Th2 cells is determined by the roles of their products, such as IL-4, IL-5, and IL-13 in the recruitment and activation of the primary effector cells of the allergic response, eosinophils, and mast cells. Activation of these cells results in the release of many inflammatory mediators that seem to induce AHR individually or coordinately (Drazen et ah, 1996 Galli, 1997), although the precise molecular mechanisms predisposing to the development of AHR in asthmatics are largely unknown. 

From the studies performed in vitro and in vivo there are several mechanisms whereby eotaxin may participate to recruit eosinophils into inflammatory sites, namely the release of eosinophils and their progenitors from the bone marrow, upregulation of adhesion molecules, chemoattraction and stimulation of other effector functions. 

Investigation of the factors associated with resistance to reinfection after praziquantel treatment of Schistosoma mansoni- and S. haematobium-mfocted populations has demonstrated correlations between parasite-specific IgE levels and resistance in a number of different studies (29-33). The mechanism by which IgE has been proposed to act is ADCC reactions in which IgE-coated parasites are attacked by effector cells including eosinophils, macrophages, and platelets (34). 

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