Schistosoma mansoni: Kinetics and class specificity of hypergammaglobulinemia induced during murine infection

Sher, Alan; McIntyre, Susan L.; Lichtenberg, F. Von

doi:10.1016/0014-4894(77)90114-x

Cited by 29 publications

(11 citation statements)

References 18 publications

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“…Despite the fact that the overall numbers of B cells in the liver did not increase dramatically by week 10 of infection (Figure 4A), there was a transition within this population in terms of IgG1 + cells such that approximately 37% of CD19 + cells at week 10 were IgG1+ compared to <2% in naïve mice (Figure 4C). Consistent with the hepatic plasma cell data and previous reports [37], schistosome egg antigen (SEA)-specific serum antibody titers were also found to increase strikingly between weeks 10 and 16 of infection (Figure 4D). Targeted measurements of antibody-secreting cells by ELISpot revealed large numbers of IgG1-secreting cells from the perfused livers of infected mice that, on a per cell basis, exceeded the number of IgG1-secreting cells from the spleens of infected animals (Figure 4E).…”

Section: Resultssupporting

confidence: 91%

IL-10R Blockade during Chronic Schistosomiasis Mansoni Results in the Loss of B Cells from the Liver and the Development of Severe Pulmonary Disease

et al. 2012

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In schistosomiasis patients, parasite eggs trapped in hepatic sinusoids become foci for CD4+ T cell-orchestrated granulomatous cellular infiltrates. Since the immune response is unable to clear the infection, the liver is subjected to ongoing cycles of focal inflammation and healing that lead to vascular obstruction and tissue fibrosis. This is mitigated by regulatory mechanisms that develop over time and which minimize the inflammatory response to newly deposited eggs. Exploring changes in the hepatic inflammatory infiltrate over time in infected mice, we found an accumulation of schistosome egg antigen-specific IgG1-secreting plasma cells during chronic infection. This population was significantly diminished by blockade of the receptor for IL-10, a cytokine implicated in plasma cell development. Strikingly, IL-10R blockade precipitated the development of portal hypertension and the accumulation of parasite eggs in the lungs and heart. This did not reflect more aggressive Th2 cell responsiveness, increased hepatic fibrosis, or the emergence of Th1 or Th17 responses. Rather, a role for antibody in the prevention of severe disease was suggested by the finding that pulmonary involvement was also apparent in mice unable to secrete class switched antibody. A major effect of anti-IL-10R treatment was the loss of a myeloid population that stained positively for surface IgG1, and which exhibited characteristics of regulatory/anti-inflammatory macrophages. This finding suggests that antibody may promote protective effects within the liver through local interactions with macrophages. In summary, our data describe a role for IL-10-dependent B cell responses in the regulation of tissue damage during a chronic helminth infection.

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Section: Resultssupporting

confidence: 91%

IL-10R Blockade during Chronic Schistosomiasis Mansoni Results in the Loss of B Cells from the Liver and the Development of Severe Pulmonary Disease

et al. 2012

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“…Total IgGl levels remain almost unchanged until day 50 after which they increase dramatically to reach a peak (day 101) that represents about 26 times the normal value. This result is similar to the one obtained by Sher et al [36]; a non-specific potentiation of IgGl homocytotropic antibody responses has been proposed as a mechanism to explain such high IgGl levels. On the contrary, se rum IgE rise earlier (between days 20 and 30) and the maximum is observed around day 50.…”

Section: Discussionsupporting

confidence: 81%

Homocytotropic Antibody Responses during Murine Schistosomiasis

Rousseaux-Prévost¹,

Bout²,

Bazin³

et al. 1980

Int Arch Allergy Immunol

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Mice infected with Schistosoma mansoni develop a high increase of homocytotropic antibodies, thought to be involved in protection. IgE and IgG1 rise differently during the course of infection. Total serum IgE levels rise between days 20 and 30 and the maximum is observed around day 50. IgG1 levels remain almost unchanged until day 50 after which they increase dramatically, reaching a peak at day 100. S. mansoni specific IgE antibodies measured by passive cutaneous anaphylaxis parallel the variations of total IgE. On the contrary, S. mansoni specific IgG1 antibodies, also measured by passive cutaneous anaphylaxis, do not parallel total IgG1; they reach a peak between days 30 and 40 and remain high until day 100.

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“…The pronounced hypergammaglobulinemia found in humans (16,26,106) and mice (251) and the occurrence of autoantibodies in the latter (134) (8,14). Proteinuria may be linked to HS disease manifestations (177,232).…”

Section: Introductionmentioning

confidence: 99%

Immunopathology of Schistosoma mansoni infection

1989

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Schistosomiasis mansoni is a chronic helminthic disease that affects about 100 million people in the tropics. The worms have a life span of 5 to 10 years, and they live in the mesenteric veins of the host. Lightly infected individuals are asymptomatic or manifest mild intestinal symptoms. Heavily infected individuals often develop severe morbidity with hepatosplenomegaly, sometimes with a fatal outcome. Morbidity is attributed to the strong humoral and T-cell-mediated host immune responses developed to a variety of parasite antigens and expressed as tissue inflammations. The immunopathology includes dermatitis, immune complex-mediated kidney disease, and, chiefly, T-cell-mediated granuloma formation and fibrosis around disseminated parasite eggs. This review describes the mechanisms of induction and expression of immunopathology in infected persons and experimental animals. Immunoregulatory mechanisms that modulate the enhanced immune responses and may ameliorate excessive morbidity are discussed.

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Schistosoma mansoni: Kinetics and class specificity of hypergammaglobulinemia induced during murine infection

Cited by 29 publications

References 18 publications

IL-10R Blockade during Chronic Schistosomiasis Mansoni Results in the Loss of B Cells from the Liver and the Development of Severe Pulmonary Disease

IL-10R Blockade during Chronic Schistosomiasis Mansoni Results in the Loss of B Cells from the Liver and the Development of Severe Pulmonary Disease

Homocytotropic Antibody Responses during Murine Schistosomiasis

Immunopathology of Schistosoma mansoni infection

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