Early development and progression of lymphocyte‐stimulatory cross‐reactive idiotypes expressed on antibodies to soluble egg antigens during <i>Schistosoma mansoni</i> infection of mice

Bosshardt, Stephen C.; Nix, Nancy A.; Colley, Daniel G.

doi:10.1002/eji.1830260143

Cited by 3 publications

(3 citation statements)

References 19 publications

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“…Although we have reported that CRI can be detected early in S. mansoni infections (21), our previous longitudinal studies of MSS and HSS mice suggested that differences between pathologic groups occurred later in infection as significant differences between anemia and serum triglyceride levels in mice that develop these distinct pathologies are not detected until 10 and 14 wk after infection, respectively (26). The current data indicate that the immunobiologic processes that determine whether or not experimental animals in this model develop severe pathology are in place very early in infection, concurrent with worm maturation and egg production.…”

Section: Resultsmentioning

confidence: 80%

Idiotypes Expressed Early in Experimental Schistosoma mansoni Infections Predict Clinical Outcomes of Chronic Disease

Montesano

Colley

Willard

et al. 2002

The Journal of Experimental Medicine

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In murine Schistosoma mansoni infections, schistosome-specific cross-reactive idiotypes (CRI) are present in the sera of mice with moderate splenomegaly syndrome (MSS) at 20 wk after infection. In contrast, sera from animals that have the more severe hypersplenomegaly syndrome (HSS) at 20 wk of infection do not express these CRI in their sera. To examine when these regulatory CRI first appear in mice that eventually develop MSS, sera from infected animals were monitored for CRI from 1.5 to 20 wk of infection. In mice that eventually developed MSS, CRI were detected by 5 to 6 wk after infection, plateaued by 8 to 10 wk, and persisted through 20 wk of infection. Animals that developed HSS pathology or that died before 20 wk of infection never expressed CRI. Moreover, CRI levels present in the sera of mice at 6 wk of infection were inversely correlated with splenomegaly and hepatic fibrosis, but not with parasitologic measures, at 20 wk after infection. These results suggest that critical events occur very early in some schistosome infections that induce the production of regulatory idiotypes and that the presence or absence of these idiotypes predicts, and possibly determines, subsequent morbidity.

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Section: Resultsmentioning

confidence: 80%

Idiotypes Expressed Early in Experimental Schistosoma mansoni Infections Predict Clinical Outcomes of Chronic Disease

Montesano

Colley

Willard

et al. 2002

The Journal of Experimental Medicine

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“…Soluble extracts of SEA or SWA have been used to study immune responses to S. mansoni [15][16][17]. To establish whether antigens within these extracts are able to influence the development of diabetes, groups of 4-week-old female NOD mice were injected once a week for 15 weeks with 50 ?…”

Section: Soluble Worm or Egg Antigens From S Mansoni Prevent Diabetementioning

confidence: 99%

Schistosoma mansoni antigens modulate the activity of the innate immune response and prevent onset of type 1 diabetes

Zaccone¹,

Fehérvari²,

Jones³

et al. 2003

Eur J Immunol

300

231

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Infection with Schistosoma mansoni (S. mansoni) or exposure to eggs from this helminth inhibits the development of type 1 diabetes in NOD mice. In this study we show that soluble extracts of S. mansoni worm or egg completely prevent onset of type 1 diabetes in these mice but only if injection is started at 4 weeks of age. T cells from diabetes-protected mice make IL-10 in recall responses to parasite antigens. These cells are furthermore impaired in their ability to transfer diabetes to NOD-SCID recipients. Bone marrow dendritic cells derived from NOD mice are found to make more IL-10 and less IL-12 following culture with S. mansoni soluble egg antigens in conjunction with lipopolysaccharides. NOD mice are deficient in NKT cells. Soluble worm and egg antigens increase the numbers of V § 14i NKT cells in NOD mice. These effects of schistosome antigens on the innate immune system provide a mechanism for their ability to prevent type 1 diabetes in NOD mice.

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“…The ability of spleen cells to proliferate in vitro was measured as previously described (Bosshardt, Nix & Colley 1996). Briefly, single cell suspensions were prepared from the spleens of uninfected mice, or mice with S. mansoni infections of eight weeks (acute) or 20-25 weeks (chronic).…”

Section: Lymphocyte Proliferationmentioning

confidence: 99%

IL‐10 deficit correlates with chronic, hypersplenomegaly syndrome in male CBA/J mice infected with Schistosoma mansoni

Bosshardt

Freeman

Secor

et al. 1997

Parasite Immunology

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Twenty weeks after moderate level infections with Schistosoma mansoni, approximately 20% of male CBA/J mice develop hypersplenomegaly syndrome (HSS) while the rest present with moderate splenomegaly syndrome (MSS). HSS and MSS mice differ pathophysiologically (degree of splenomegaly, anaemia, ascites, periportal fibrosis, portal hypertension) and immunologically with regard to antibodies (idiotypic expression, isotype levels) to schistosome soluble egg antigens (SEA), and spleen cell phenotypic profiles. This study compared in vitro proliferative responses and IL-2, IFN gamma, IL-4, and IL-10 production by spleen cells from uninfected mice and mice with acute (8 wk), MSS or HSS schistosomiasis mansoni, upon exposure to anti-CD3 epsilon or SEA, Spleen cells from uninfected mice produce Il-2 to anti-CD3 epsilon but exposure of cells from all three groups of infected mice to anti-CD3 epsilon or SEA led to only very low levels of supernatant IL-2. Anti-CD3 epsilon- or SEA-stimulated production of IFN gamma or Il-4, and anti-CD3 epsilon-stimulated production of IL-10, displayed similar patterns: highest cytokine production by cells from mice with acute infections and lower levels of production that did not differ between the two chronic groups. In contrast, while SEA-stimulated IL-10 production was again highest with cells from mice with acute infections, spleen cells from mice with MSS produced significantly more IL-10 than did those from mice with HSS. This association of low levels of antigen-induced IL-10 with severe pathology is consistent with the theory that IL-10 plays a role in the immunoregulation that occurs in chronic schistosomiasis.

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Early development and progression of lymphocyte‐stimulatory cross‐reactive idiotypes expressed on antibodies to soluble egg antigens during Schistosoma mansoni infection of mice

Cited by 3 publications

References 19 publications

Idiotypes Expressed Early in Experimental Schistosoma mansoni Infections Predict Clinical Outcomes of Chronic Disease

Idiotypes Expressed Early in Experimental Schistosoma mansoni Infections Predict Clinical Outcomes of Chronic Disease

Schistosoma mansoni antigens modulate the activity of the innate immune response and prevent onset of type 1 diabetes

IL‐10 deficit correlates with chronic, hypersplenomegaly syndrome in male CBA/J mice infected with Schistosoma mansoni

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