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SPECIFIC IMMUNE RESPONSES TO PARASI
SPECIFIC IMMUNE RESPONSES TO PARASITES
It is difficult to generalize about the mechanisms of antiparasitic immunity because there are many different parasites that have different forms and reside in different tissue locations during their life cycles (Table 10-4). Stimulation of CD4 TH1, TH17, CD8 T-cell, and macrophage responses are important for intracellular infections, and TH2 antibody responses are important for extracellular parasites in blood and fluids. IgE, eosinophil, and mast cell action are especially important for eliminating worm (cestode and nematode) infections. The efficiency of control of the infection may depend on which response is initiated in the host. Dominance of a TH2 response to Leishmania infections results in the inhibition of TH1 activation of macrophages, inability to clear intracellular parasites, and a poor outcome. This observation provided the basis for the discovery that TH1 and TH2 responses are separate and antagonistic. Parasites have developed sophisticated mechanisms for avoiding immune clearance and often establish chronic infections.
Extracellular parasites, such as Trypanosoma cruzi, Toxoplasma gondii, and Leishmania species, are phagocytosed by macrophage. Antibody may facilitate the uptake of (opsonize) the parasites. Killing of the parasites follows activation of the macrophage by IFN-γ (produced by NK, γ/δ T, or CD4 TH1 cells) or TNF-α (produced by other macrophages) and induction of oxygen-dependent killing mechanisms (peroxide, superoxide, nitric oxide). The parasites may replicate in the macrophage and hide from subsequent immune detection unless the macrophage is activated by TH1 responses.
TH1 production of IFN-γ and activation of macrophages are also essential for defense against intracellular protozoa and for the development of granulomas around Schistosoma mansoni eggs and worms in the liver. The granuloma, formed by layers of inflammatory cells, protects the liver from toxins produced by the eggs. However, the granuloma also causes fibrosis, which interrupts the venous blood supply to the liver, leading to hypertension and cirrhosis.
It is difficult to generalize about the mechanisms of antiparasitic immunity because there are many different parasites that have different forms and reside in different tissue locations during their life cycles (Table 10-4). Stimulation of CD4 TH1, TH17, CD8 T-cell, and macrophage responses are important for intracellular infections, and TH2 antibody responses are important for extracellular parasites in blood and fluids. IgE, eosinophil, and mast cell action are especially important for eliminating worm (cestode and nematode) infections. The efficiency of control of the infection may depend on which response is initiated in the host. Dominance of a TH2 response to Leishmania infections results in the inhibition of TH1 activation of macrophages, inability to clear intracellular parasites, and a poor outcome. This observation provided the basis for the discovery that TH1 and TH2 responses are separate and antagonistic. Parasites have developed sophisticated mechanisms for avoiding immune clearance and often establish chronic infections.
Extracellular parasites, such as Trypanosoma cruzi, Toxoplasma gondii, and Leishmania species, are phagocytosed by macrophage. Antibody may facilitate the uptake of (opsonize) the parasites. Killing of the parasites follows activation of the macrophage by IFN-γ (produced by NK, γ/δ T, or CD4 TH1 cells) or TNF-α (produced by other macrophages) and induction of oxygen-dependent killing mechanisms (peroxide, superoxide, nitric oxide). The parasites may replicate in the macrophage and hide from subsequent immune detection unless the macrophage is activated by TH1 responses.
TH1 production of IFN-γ and activation of macrophages are also essential for defense against intracellular protozoa and for the development of granulomas around Schistosoma mansoni eggs and worms in the liver. The granuloma, formed by layers of inflammatory cells, protects the liver from toxins produced by the eggs. However, the granuloma also causes fibrosis, which interrupts the venous blood supply to the liver, leading to hypertension and cirrhosis.
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特异性免疫反应寄生虫<br>这是很难概括抗寄生虫药免疫的机制，因为存在具有不同的形式和在它们的生命周期（表10-4）驻留在不同的组织位置许多不同的寄生虫。CD4 TH1，TH17，CD8 T细胞的刺激，和巨噬细胞应答是细胞内感染重要的是，和TH2抗体应答是用于在血液和体液的细胞外寄生虫重要。的IgE，嗜酸性粒细胞和肥大细胞作用是消除蠕虫（绦虫和线虫）感染尤为重要。感染控制的效率可以依赖于其中响应在主机发起。在TH1活化巨噬细胞，无法清除细胞内寄生虫和预后不良的抑制Th2应答对Leishmania感染的结果主导地位。这一观察提供了发现TH1和TH2反应是分开的，对立的基础。寄生虫已经制定了避免免疫清除成熟的机制，常常建立慢性感染。<br>胞外寄生虫，如克氏锥虫，弓形虫，和利什曼原虫属物种中，通过巨噬细胞吞噬。抗体可以促进（调理）寄生虫摄取。寄生虫杀伤遵循由IFN-γ的巨噬细胞的活化（通过NK产生，γ/δT，或CD4 TH1细胞）或TNF-α（由其他巨噬细胞产生）和氧依赖性杀伤机制（过氧化诱导，超氧， 一氧化氮）。寄生虫也可以在巨噬细胞进行复制，从随后的免疫检测隐藏除非巨噬细胞是由Th1应答激活。<br>TH1产生IFN-γ和巨噬细胞的激活也是对细胞内原虫国防和周边的曼氏血吸虫卵肉芽肿和蠕虫在肝脏的发展至关重要。肉芽肿，炎症细胞的层而形成，可防止由卵产生的毒素肝脏。然而，肉芽肿也导致纤维化，从而中断了静脉血液供应到肝脏，导致高血压和肝硬化。
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对寄生者的具体回复<br>很难概括抗寄生虫免疫机制，因为有许多不同的寄生虫，它们有不同的形式，在生命周期中存在于不同的组织位置（表10-4）。CD4 TH1、TH17、CD8 T细胞和巨噬细胞反应的刺激对细胞内感染很重要，TH2抗体反应对血液和液体中的细胞外寄生虫很重要。IgE、嗜酸性粒细胞和乳腺细胞作用对于消除蠕虫（虫病和线虫）感染尤为重要。控制感染的效率可能取决于在主机中启动响应。TH2对利什曼病感染反应的主导地位导致抑制TH1激活巨噬细胞，无法清除细胞内寄生虫，结果不佳。这一观察为发现TH1和TH2反应是分开和对抗提供了依据。寄生虫已经开发出了避免免疫清除的精密机制，并经常建立慢性感染。<br>细胞外寄生虫，如锥形瘤、弓形虫和利什曼病物种，被巨噬细胞噬菌体噬菌体噬菌体。抗体可促进寄生虫的摄入（化原体）。在通过IFN-*（由NK、+/+T或CD4 TH1细胞产生）或TNF-α（由其他巨噬细胞产生）和诱导氧依赖性杀灭机制（过氧化物、超氧化物、一氧化氮）激活巨噬细胞之前，杀死寄生虫。寄生虫可能在巨噬菌体中复制，并隐藏在随后的免疫检测，除非巨噬菌体被TH1反应激活。<br>TH1 IFN-α的产生和巨噬细胞的活化对于防御细胞内原生动物和在血吸虫卵和肝脏蠕虫周围发展肉芽肿也是必不可少的。由炎症细胞层形成的肉芽肿保护肝脏免受卵子产生的毒素的侵害。然而，肉芽肿也会导致纤维化，中断静脉血液供应到肝脏，导致高血压和肝硬化。
正在翻译中..
寄生虫特异性免疫反应<br>抗寄生虫免疫的机制很难一概而论，因为有许多不同的寄生虫有不同的形式，在它们的生命周期中居住在不同的组织位置（表10-4）。刺激cd4-th1、th17、cd8-t细胞和巨噬细胞反应对细胞内感染很重要，而th2抗体反应对血液和体液中的细胞外寄生虫很重要。ige、嗜酸性粒细胞和肥大细胞的作用对于消除蠕虫（绦虫和线虫）感染尤其重要。感染的控制效率可能取决于在宿主中启动的反应。利什曼原虫感染后th2反应的优势导致巨噬细胞th1激活受到抑制，无法清除细胞内寄生虫，结果不佳。这一观察结果为发现th1和th2反应是分离的和拮抗的提供了基础。寄生虫已经发展出复杂的机制，以避免免疫清除，并往往建立慢性感染。<br>细胞外寄生虫，如cruzi锥虫、弓形虫和利什曼原虫，被巨噬细胞吞噬。抗体可促进寄生虫的吸收。寄生虫的杀灭是通过ifn-γ（由nk、γ/δt或cd4-th1细胞产生）或tnf-α（由其他巨噬细胞产生）激活巨噬细胞，并诱导氧依赖性杀灭机制（过氧化物、超氧化物、一氧化氮）来实现的。除非巨噬细胞被th1反应激活，否则寄生虫可能在巨噬细胞中复制并隐藏起来，以防随后的免疫检测。<br>产生ifn-γ的th1和巨噬细胞的激活对于防御细胞内原生动物和肝脏曼氏血吸虫卵和蠕虫周围肉芽肿的发展也是必不可少的。肉芽肿是由层层炎症细胞形成的，它保护肝脏免受鸡蛋产生的毒素的侵害。然而，肉芽肿也会导致纤维化，从而中断肝脏的静脉血供应，导致高血压和肝硬化。<br>
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