Analysis of the peripheral immune response in patients with neurocysticercosis: evidence for T cell reactivity to parasite glycoprotein and vesicular fluid antigens.

Restrepo, Blanca I.; Aguilar, Maria I.; Melby, Peter C.; Teale, Judy M.

doi:10.4269/ajtmh.2001.65.366

Cited by 28 publications

(21 citation statements)

References 15 publications

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“…This study focused on specimens that had a granuloma surrounding brain cysticerci. Despite the previously documented heterogeneity of cellular and humoral immune responses among patients with NCC, in the present study a consistent in situ response was observed in eight cases where granulomas surrounded brain cysticerci (21,28,29). Essentially, each specimen contained a dead and disintegrating parasite that was surrounded by an immune granuloma with intense fibrosis, inflammation, and angiogenesis.…”

Section: Discussionmentioning

confidence: 63%

Brain Granulomas in Neurocysticercosis Patients Are Associated with a Th1 and Th2 Profile

et al. 2001

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Neurocysticercosis (NCC) is a common central nervous system (CNS) infection caused by Taenia solium metacestodes. Despite the well-documented importance of the granulomatous response in the pathogenesis of this infection, there is limited information about the types of cells and cytokines involved. In fact, there has been limited characterization of human brain granulomas with any infectious agent. In the present study a detailed histological and immunohistochemical analysis of the immune response was performed on eight craniotomy specimens where a granuloma surrounded each T. solium metacestode. The results indicated that in all the specimens there was a dying parasite surrounded by a mature granuloma with associated fibrosis, angiogenesis, and an inflammatory infiltrate. The most abundant cell types were plasma cells, B and T lymphocytes, macrophages, and mast cells. Th1 cytokines were prevalent and included gamma interferon, interleukin-18 (IL-18), and the immunosuppressive, fibrosis-promoting cytokine transforming growth factor ␤. The Th2 cytokines IL-4, IL-13, and IL-10 were also present. These observations indicate that a chronic immune response is elicited in the CNS environment with multiple cell types that together secrete inflammatory and anti-inflammatory cytokines. In addition, both collagen type I and type III deposits were evident and could contribute to irreversible nervous tissue damage in NCC patients.

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Section: Discussionmentioning

confidence: 63%

Brain Granulomas in Neurocysticercosis Patients Are Associated with a Th1 and Th2 Profile

et al. 2001

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“…Thus, genetic, immunological, and hormonal factors have been related to resistance in this model (14,15,20,22,31,41). Likewise, some of these observations have been confirmed in the natural hosts for T. solium (30,33,34).…”

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confidence: 68%

Macrophage Migration Inhibitory Factor Plays a Critical Role in Mediating Protection against the Helminth ParasiteTaenia crassiceps

et al. 2003

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To determine the role of endogenous migration inhibitory factor (MIF) in regulation of immune response during murine cysticercosis caused by the helminth parasite Taenia crassiceps, we analyzed the course of T. crassiceps infection in MIF ؊/؊ BALB/c mice. MIF ؊/؊ mice were highly susceptible to T. crassiceps and developed significantly higher parasite loads compared to similarly infected MIF ؉/؉ mice. Throughout the course of infection, Taenia crassiceps soluble antigen-stimulated spleen cells from both MIF ؉/؉ and MIF ؊/؊ mice produced significant and comparable levels of interleukin-4 (IL-4), but those from MIF ؊/؊ mice produced significantly more IL-13, as well as gamma interferon (IFN-␥), suggesting that the susceptibility of MIF ؊/؊ mice to T. crassiceps was not due to the lack of IFN-␥ production. Interestingly, low levels of both total and specific immunoglobulin G2a were observed in MIF ؊/؊ cysticercotic mice despite the high IFN-␥ levels; in addition, peritoneal macrophages obtained from T. crassiceps-infected MIF ؊/؊ mice at different time points failed to respond efficiently to stimulation in vitro with lipopolysaccharide plus IFN-␥ and produced significantly lower levels of IL-12, tumor necrosis factor alpha, and NO compared to those from MIF ؉/؉ mice. These findings demonstrate that MIF plays a critical role in mediating protection against T. crassiceps in vivo. Moreover, these findings also suggest that impaired macrophage function rather than the lack of Th1 development may be responsible for mediating susceptibility to T. crassiceps.

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“…Considering the relevance of neuroinXammation in NC pathogenesis, increased eVorts have been performed to characterize the immune-inXammatory response in NC and its role in dealing with the parasite [9][10][11][12][13][14][15][16][17]. All studies have been performed studying the CSF (local) or blood (peripheral) of NC patients independently.…”

Section: Introductionmentioning

confidence: 99%

Neurocysticercosis: local and systemic immune-inflammatory features related to severity

Sáenz¹,

Fleury²,

Chavarría³

et al. 2011

Med Microbiol Immunol

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Neurocysticercosis (NC) is caused by the establishment of Taenia solium cysticerci in the central nervous system. Previous studies have established that neuroinflammation plays a key role in the severity of the disease. However, the relationship between peripheral and local immune response remains inconclusive. This work studies the peripheral and local immune-inflammatory features and their relationships, toward the identification of potential peripheral immunologic features related to severity. A panel of cytokines was measured in paired cerebrospinal fluid (CSF) and in the supernatant of antigen-specific stimulated peripheral blood mononuclear cells samples (SN) in a total of 31 untreated inflammatory and non-inflammatory NC patients. Increased clinical and radiologic severity was associated with an increased cerebrospinal fluid cell count. A peripheral proliferative depression that negatively correlates with CSF cellularity and TNFα and that positively correlates with SN IL5 was observed in severe NC patients. These results provide evidences to support the systemic proliferative response as a biomarker to monitor the level of neuroinflammation, of possible value in the patients' follow-up during treatment.

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Analysis of the peripheral immune response in patients with neurocysticercosis: evidence for T cell reactivity to parasite glycoprotein and vesicular fluid antigens.

Cited by 28 publications

References 15 publications

Brain Granulomas in Neurocysticercosis Patients Are Associated with a Th1 and Th2 Profile

Brain Granulomas in Neurocysticercosis Patients Are Associated with a Th1 and Th2 Profile

Macrophage Migration Inhibitory Factor Plays a Critical Role in Mediating Protection against the Helminth ParasiteTaenia crassiceps

Neurocysticercosis: local and systemic immune-inflammatory features related to severity

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