Cellular Immune Response and Th1/Th2 Cytokines in Human Neurocysticercosis: Lack of Immune Suppression

Medina-Escutia, Edith; Morales-López, Zoila; Proaño, Jefferson V.; Vázquez, José Ramón Parada; Bermúdez, Victor; Ortı́z-Navarrete, Vianney; Madrid‐Marina, Vicente; Laclette, Juan Pedro; Correa, Dolores

doi:10.1645/0022-3395(2001)087[0587:ciratt]2.0.co;2

Cited by 18 publications

(7 citation statements)

References 18 publications

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“…Likewise, dendritic cells stimulated with helminth components show limited upregulation of CD80, CD86 and MHC-II expression in comparison to the expression induced by bacterial antigens [37]. In some studies has been shown that NCC patients exhibit a depressed peripheral cellular immune response [38], although this is controversial [39],[40]. In other helminth infections, results indicate that released products may interfere with the generation of pro-inflammatory mediators [41], the antigen presentation process [42] and other immune defense mechanisms elicited by the host upon helminth infection [3],[43],[44].…”

Section: Discussionmentioning

confidence: 99%

Differential Release and Phagocytosis of Tegument Glycoconjugates in Neurocysticercosis: Implications for Immune Evasion Strategies

2008

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Neurocysticercosis (NCC) is an infection of the central nervous system (CNS) by the metacestode of the helminth Taenia solium. The severity of the symptoms is associated with the intensity of the immune response. First, there is a long asymptomatic period where host immunity seems incapable of resolving the infection, followed by a chronic hypersensitivity reaction. Since little is known about the initial response to this infection, a murine model using the cestode Mesocestoides corti (syn. Mesocestoides vogae) was employed to analyze morphological changes in the parasite early in the infection. It was found that M. corti material is released from the tegument making close contact with the nervous tissue. These results were confirmed by infecting murine CNS with ex vivo–labeled parasites. Because more than 95% of NCC patients exhibit humoral responses against carbohydrate-based antigens, and the tegument is known to be rich in glycoconjugates (GCs), the expression of these types of molecules was analyzed in human, porcine, and murine NCC specimens. To determine the GCs present in the tegument, fluorochrome-labeled hydrazides as well as fluorochrome-labeled lectins with specificity to different carbohydrates were used. All the lectins utilized labeled the tegument. GCs bound by isolectinB4 were shed in the first days of infection and not resynthesized by the parasite, whereas GCs bound by wheat germ agglutinin and concavalinA were continuously released throughout the infectious process. GCs bound by these three lectins were taken up by host cells. Peanut lectin-binding GCs, in contrast, remained on the parasite and were not detected in host cells. The parasitic origin of the lectin-binding GCs found in host cells was confirmed using antibodies against T. solium and M. corti. We propose that both the rapid and persistent release of tegumental GCs plays a key role in the well-known immunomodulatory effects of helminths, including immune evasion and life-long inflammatory sequelae seen in many NCC patients.

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Section: Discussionmentioning

confidence: 99%

Differential Release and Phagocytosis of Tegument Glycoconjugates in Neurocysticercosis: Implications for Immune Evasion Strategies

2008

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“…Table 2 ( 120–135) shows the immunologic actors associated with the different clinical or radiological phenotypes of NC. From necropsies come the harder data on the immunological actors involved in the inflammatory process in NC.…”

Section: The Immune Response In Human Neurocysticercosismentioning

confidence: 99%

The immune response in Taenia solium cysticercosis: protection and injury

Sciutto

Chavarría

Fragoso

et al. 2007

Parasite Immunology

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“…Data are consistent with other observations indicating that innate and adaptive arms of the host-immune response may be downregulated in response to T. solium (42, 44, 50, 51). In contrast, there was no evidence of immune suppression in Con A-stimulated PBMCs from NCC patients compared with controls (52), and active peripheral immunity was reported in NCC patients (53). The effect on plasma TNF-α and CXCL8 concentrations was relatively specific, with no detectable changes in the peripheral concentrations of a broad range of proinflammatory cytokines or their inhibitors in NCC patients.…”

Section: Discussionmentioning

confidence: 89%

Mechanisms Regulating Monocyte CXCL8 Secretion in Neurocysticercosis and the Effect of Antiparasitic Therapy

Uddin

González

Gilman

et al. 2010

The Journal of Immunology

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Neurocysticercosis (NCC) due to infection with Taenia solium is a major cause of epilepsy worldwide. Larval degeneration, which may follow antiparasitic treatment, results in clinical symptoms due to inflammatory cell influx. Mechanisms regulating this are not well understood, but chemokines have a key role. Stimulation of human monocytes by cyst Ags from NCC-infected pigs showed that scolex and membrane Ags drive CXCL8 and CCL2 secretion. Antiparasitic treatment of pigs increased CXCL8 in response to brain, but not muscle, cyst Ags. Cyst-fluid Ags did not elicit monocyte chemokine secretion, inhibited LPS-induced CXCL8 by up to 89%, but did not alter CCL2 secretion. This effect was inhibited by anti–IL-10 Abs. Plasma CXCL8, TNF-α, IL-10, eotaxin, IL-1, IL-1ra, soluble IL-1R-II, and soluble TNFR-I and -II levels were evaluated in 167 NCC patients. Patients had lower plasma CXCL8 and TNF-α concentrations than control subjects. In summary, larval Ags from brain and muscle cysts differentially regulate chemokine secretion. Cyst-fluid inhibits CXCL8, and this is blocked by anti–IL-10 Abs. CXCL8 concentrations are decreased in patient plasma. Following anti-parasitic therapy, scolex and membrane Ags are exposed, and cyst fluid is decreased, leading to inflammatory cell influx. Taken together, the cellular, porcine, and human data may explain, in part, why NCC is usually asymptomatic but may cause proinflammatory symptoms, particularly following treatment.

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Cellular Immune Response and Th1/Th2 Cytokines in Human Neurocysticercosis: Lack of Immune Suppression

Cited by 18 publications

References 18 publications

Differential Release and Phagocytosis of Tegument Glycoconjugates in Neurocysticercosis: Implications for Immune Evasion Strategies

Differential Release and Phagocytosis of Tegument Glycoconjugates in Neurocysticercosis: Implications for Immune Evasion Strategies

The immune response in Taenia solium cysticercosis: protection and injury

Mechanisms Regulating Monocyte CXCL8 Secretion in Neurocysticercosis and the Effect of Antiparasitic Therapy

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