Lack of C3 Affects Th2 Response Development and the Sequelae of Chemotherapy in Schistosomiasis

Flamme, Anne Camille La; MacDonald, Andrew S.; Huxtable, C. R.; Carroll, Michael; Pearce, Edward J.

doi:10.4049/jimmunol.170.1.470

Cited by 37 publications

(28 citation statements)

References 61 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The cytokine results were reflected in the Ab responses, in that IgG1 responses in C3 Ϫ/Ϫ mice were significantly impaired, IgG2a responses were unaffected, and infected C3 Ϫ/Ϫ mice actually had increased production of parasite-specific IgM (8). In the current study, C3…”

Section: Discussionmentioning

confidence: 84%

Complement Component C3 Is Required for Protective Innate and Adaptive Immunity to Larval Strongyloides stercoralis in Mice

Kerepesi

Hess

Nolan

et al. 2006

The Journal of Immunology

View full text Add to dashboard Cite

This study examines the role of complement components C3 and C5 in innate and adaptive protective immunity to larval Strongyloides stercoralis in mice. Larval survival in naive C3−/− mice was increased as compared with survival in wild-type mice, whereas C3aR−/− and wild-type mice had equivalent levels of larval killing. Larval killing in naive mice was shown to be a coordinated effort between effector cells and C3. There was no difference between survival in wild-type and naive C5−/− mice, indicating that C5 was not required during the innate immune response. Naive B cell-deficient and wild-type mice killed larvae at comparable levels, suggesting that activation of the classical complement pathway was not required for innate immunity. Adaptive immunity was equivalent in wild-type and C5−/− mice; thus, C5 was also not required during the adaptive immune response. Larval killing was completely ablated in immunized C3−/− mice, even though the protective parasite-specific IgM response developed and effector cells were recruited. Protective immunity was restored to immunized C3−/− mice by transferring untreated naive serum, but not C3-depleted heat-inactivated serum to the location of the parasites. Finally, immunized C3aR−/− mice killed larvae during the adaptive immune response as efficiently as wild-type mice. Therefore, C3 was not required for the development of adaptive immunity, but was required for the larval killing process during both protective innate and adaptive immune responses in mice against larval S. stercoralis.

show abstract

Section: Discussionmentioning

confidence: 84%

Complement Component C3 Is Required for Protective Innate and Adaptive Immunity to Larval Strongyloides stercoralis in Mice

Kerepesi

Hess

Nolan

et al. 2006

The Journal of Immunology

View full text Add to dashboard Cite

show abstract

“…Clinical scores of morbidity were assessed 48 hours after PHx, as previously described (56). Each mouse was graded from 0 to 3 (normal, 0; slight effect, 1; moderate effect, 2; severe effect, 3) for posture, coat, and activity, and scores combined to a final score on a scale from 0 to 9.…”

Section: Methodsmentioning

confidence: 99%

A complement-dependent balance between hepatic ischemia/reperfusion injury and liver regeneration in mice

He¹,

Atkinson²,

Qiao³

et al. 2009

J. Clin. Invest.

125

View full text Add to dashboard Cite

Massive liver resection and small-for-size liver transplantation pose a therapeutic challenge, due to increased susceptibility of the remnant/graft to ischemia reperfusion injury (IRI) and impaired regeneration. We investigated the dual role of complement in IRI versus regeneration in mice. Complement component 3 (C3) deficiency and complement inhibition with complement receptor 2-complement receptor 1-related protein y (CR2-Crry, an inhibitor of C3 activation) provided protection from hepatic IRI, and while C3 deficiency also impaired liver regeneration following partial hepatectomy (PHx), the effect of CR2-Crry in this context was dose dependent. In a combined model of IRI and PHx, either C3 deficiency or high-dose CR2-Crry resulted in steatosis, severe hepatic injury, and high mortality, whereas low-dose CR2-Crry was protective and actually increased hepatic proliferative responses relative to control mice. Reconstitution experiments revealed an important role for the C3a degradation product acylation-stimulating protein (ASP) in the balance between inflammation/injury versus regeneration. Furthermore, liver regeneration was dependent on the putative ASP receptor, C5L2. Several potential mechanisms of hepatoprotection and recovery were identified in mice treated with low-dose CR2-Crry, including enhanced IL-6 expression and STAT3 activation, reduced hepatic ATP depletion, and attenuated oxidative stress. These data indicate that a threshold of complement activation, involving ASP and C5L2, promotes liver regeneration and suggest a balance between complement-dependent injury and regeneration.

show abstract

“…Recombinant TNF-␣ occasionally did not restore HG formation (24), suggesting that this cytokine was only marginally required. Table 4 shows that infected mice with KO of some genes for (81). Eight weeks after mice deficient in the third component (C3) of complement were infected with S. mansoni, SEA-specific Th2 cytokine (IL-5, Il-6, IL-10, IL-13) production by the SC was significantly reduced.…”

Section: Granuloma Formationmentioning

confidence: 99%

Regulation of Granulomatous Inflammation in Experimental Models of Schistosomiasis

Stavitsky

2004

Infect Immun

View full text Add to dashboard Cite

Lack of C3 Affects Th2 Response Development and the Sequelae of Chemotherapy in Schistosomiasis

Cited by 37 publications

References 61 publications

Complement Component C3 Is Required for Protective Innate and Adaptive Immunity to Larval Strongyloides stercoralis in Mice

Complement Component C3 Is Required for Protective Innate and Adaptive Immunity to Larval Strongyloides stercoralis in Mice

A complement-dependent balance between hepatic ischemia/reperfusion injury and liver regeneration in mice

Regulation of Granulomatous Inflammation in Experimental Models of Schistosomiasis

Contact Info

Product

Resources

About