Murine schistosomiasis mansoni: coordinate cytokine regulation and differences in cellular immune responses of granuloma cells and splenocytes to endogenous and exogenous schistosome egg antigens

King, Christopher L.; Xianli, Jia; Stavitsky, Abram B.

doi:10.1046/j.1365-3024.2001.00420.x

Cited by 14 publications

(21 citation statements)

References 36 publications

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“…6C). This was consistent with previous observations of the development of SEA-reactive lymphocytes in the spleen before their detection in granuloma-infiltrating cells (39). Phillips and coworkers (40) have also shown that activated cells home to granulomas, although they did not address the role of Ag specificity.…”

Section: Figure 8 Absence Of S Mansoni-induced Liver Granuloma Formsupporting

confidence: 92%

“…Phillips and coworkers (40) have also shown that activated cells home to granulomas, although they did not address the role of Ag specificity. Both groups found that splenic lymphocytes have a higher proliferative capacity, suggesting that both systemic expansion and activation play a role in the recruitment of lymphocytes to granulomatous sites (39,40).…”

Section: Figure 8 Absence Of S Mansoni-induced Liver Granuloma Formmentioning

confidence: 99%

“…On the one hand, Ag-specific T cells may dominate locally. Systemic and local Ag leads to activation and expansion of parasite-specific T cells (39,40) which home to the granuloma and are preferentially retained and expanded. This model is supported by data showing that SEA-reactive lymphocytes are recruited to granulomas in vivo (42) and by in vivo identification of immunodominant T cell epitopes from SEA (30).…”

Section: Figure 8 Absence Of S Mansoni-induced Liver Granuloma Formmentioning

confidence: 99%

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CD4+ TCR Repertoire Heterogeneity inSchistosoma mansoni-Induced Granulomas

Hogan

Wang

Suresh

et al. 2002

The Journal of Immunology

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The hallmark of Schistosoma mansoni infection is the formation of liver granulomas around deposited ova. The initiation of granuloma formation is T cell-dependent since granulomas are not formed in their absence. We investigated whether a few T cells arrive to initiate the inflammatory lesion and subsequently expand locally, or whether a large repertoire of systemically activated T cells home to the delayed type hypersensitivity reaction induced by the ova. The TCR repertoire of single granulomas from the same liver were analyzed by PCR using Vβ-specific primers and CDR3 analysis. Each granuloma has a very diverse TCR repertoire indicating that most of the T cells recruited to these lesions are activated systemically. At the same time, sequence analysis of individually sized CDR3 products from single granuloma indicate that a fraction of T cells expand locally at the lesion site. Using TCR transgenic mice containing a pigeon cytochrome c-specific T cell population or lymphocytic choriomeningitis virus infection tracked with lymphocytic choriomeningitis virus-specific tetramers, we demonstrated that nonspecific T cells home to the granuloma if they are activated. However, recombinase-activating gene 2−/− pigeon cytochrome c-specific TCR transgenic mice fail to form granulomas in response to S. mansoni ova even after T cell activation, suggesting a requirement for egg-specific T cells in the initiation of these inflammatory lesions. Understanding the mechanism of T cell recruitment into granulomas has important implications for the rational design of immunotherapies for granulomatous diseases.

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Section: Figure 8 Absence Of S Mansoni-induced Liver Granuloma Formsupporting

confidence: 92%

Section: Figure 8 Absence Of S Mansoni-induced Liver Granuloma Formmentioning

confidence: 99%

Section: Figure 8 Absence Of S Mansoni-induced Liver Granuloma Formmentioning

confidence: 99%

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CD4+ TCR Repertoire Heterogeneity inSchistosoma mansoni-Induced Granulomas

Hogan

Wang

Suresh

et al. 2002

The Journal of Immunology

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“…31 High levels of IL-4 endogenously produced by the egg granuloma cells 69 could inhibit proliferation of Th1 cells. High levels of IL-10 produced by regulatory CD4 ϩ CD25 ϩ cells and macrophages in the granulomas can inhibit both Th2 and Th1 responses 69 -72 and the abundant alternatively activated macrophages are crucial in preventing severe Th1-dependent inflammatory disease.…”

Section: Discussionmentioning

confidence: 99%

The Schistosoma mansoni Hepatic Egg Granuloma Provides a Favorable Microenvironment for Sustained Growth of Leishmania donovani

Hassan

Zhang

Engwerda

et al. 2006

The American Journal of Pathology

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Parasitic co-infections are prevalent in many parts of the world. However, relatively little is known about how an underlying infection may impact on the host's ability to control a newly acquired parasite, especially if both infect the same organ. We have studied this using an experimental co-infection model in C57BL/6 mice involving Schistosoma mansoni and Leishmania donovani, two important human pathogens affecting the liver. We show that mice with established S. mansoni infections fail to control L. donovani growth in the liver and spleen. The failure occurs despite the development of a functional anti-L. donovani Th1 response that can mediate granuloma formation and effective clearance of amastigotes from foci of infection in the hepatic parenchyma. Instead, anti-leishmanial immunity fails within the S. mansoni egg granuloma, consistent with a lack of L. donovani granuloma assembly in this tissue microenvironment and consequent lack of NO production. Persisting amastigote replication in the S. mansoni egg granulomas may thus explain the increased L. donovani burden in the liver and spleen. These results may have implications for human S. mansoni and L. donovani co-infections and also demonstrate that granulomatous tissue responses to helminth organisms can form a discrete niche facilitating survival of intracellular pathogens.

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“…Somular antigens which cross-react with SEA (85) must induce this early development and expansion of SEA-reactive lymphocytes. Thus, in a mouse 4 weeks postinfection, when egg laying begins and several weeks before HG appear, SEA-reactive lymphocytes are primed and proliferate in the spleen (78). These SEA-reactive lymphoblasts are then recruited into the HG (121).…”

Section: Granuloma Formationmentioning

confidence: 99%

Murine schistosomiasis mansoni: coordinate cytokine regulation and differences in cellular immune responses of granuloma cells and splenocytes to endogenous and exogenous schistosome egg antigens

Cited by 14 publications

References 36 publications

CD4+ TCR Repertoire Heterogeneity inSchistosoma mansoni-Induced Granulomas

CD4+ TCR Repertoire Heterogeneity inSchistosoma mansoni-Induced Granulomas

The Schistosoma mansoni Hepatic Egg Granuloma Provides a Favorable Microenvironment for Sustained Growth of Leishmania donovani

Regulation of Granulomatous Inflammation in Experimental Models of Schistosomiasis

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