Apoptotic Cells at the Crossroads of Tolerance and Immunity

Škoberne, Mojca; Beignon, Anne-Sophie; Larsson, Marie; Bhardwaj, Nina

doi:10.1007/3-540-27320-4_12

Cited by 50 publications

(66 citation statements)

References 223 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…CD44-mediated phagocytosis of beads also induces inside-out activation of complement receptor 3 (CR3; CD11b/CD18 complex) (50), and we and others have reported that signaling through CR3 can inhibit DC function (22,27,51). CD44 also has been shown to negatively regulate TLR signaling and subsequent inflammation due to the fact that Cd44 -/-mice exhibit increased NF-κB signaling, proinflammatory cytokine production by TLR-stimulated macrophages, and consequentially more severe TLR-induced arthritis (52).…”

Section: Figurementioning

confidence: 99%

HIV-1 infection–induced apoptotic microparticles inhibit human DCs via CD44

Frleta¹,

Ochoa²,

Kramer³

et al. 2012

J. Clin. Invest.

View full text Add to dashboard Cite

Acute HIV-1 infection results in dysregulated immunity, which contributes to poor control of viral infection. DCs are key regulators of both adaptive and innate immune responses needed for controlling HIV-1, and we surmised that factors elicited during acute HIV-1 infection might impede DC function. We derived immature DCs from healthy donor peripheral blood monocytes and treated them with plasma from uninfected control donors and donors with acute HIV-1 infections. We found that the plasma from patients with HIV specifically inhibited DC function. This suppression was mediated by elevated apoptotic microparticles derived from dying cells during acute HIV-1 infection. Apoptotic microparticles bound to and inhibited DCs through the hyaluronate receptor CD44. These data suggest that targeting this CD44-mediated inhibition by apoptotic microparticles could be a novel strategy to potentiate DC activation of HIV-specific immunity.

show abstract

Section: Figurementioning

confidence: 99%

HIV-1 infection–induced apoptotic microparticles inhibit human DCs via CD44

Frleta¹,

Ochoa²,

Kramer³

et al. 2012

J. Clin. Invest.

View full text Add to dashboard Cite

show abstract

“…Potential mechanisms of the direct interactions between mast cell and endostatin remain hypothetical. Potentially, endostatin may interact with integrins a5b1 and avb3, expressed by both mast cells (Columbo et al, 1995;Columbo and Bochner, 2001) and DCs (Jancic et al, 1998;Skoberne et al, 2005), which also serve as binding partners for endostatin in endothelial cells (Rehn et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

172: Serum endostatin levels are elevated in colorectal cancer and correlate with invasion and systemic inflammatory markers

Tuomisto¹,

Kantola²,

Väyrynen³

et al. 2014

European Journal of Cancer

View full text Add to dashboard Cite

“…It has been demonstrated that apoptotic cells and necrotic cells play distinct roles in regulating immune responses [19,20]. Apoptotic cells induce immune tolerance whereas necrotic cells activate immune response [17].…”

Section: Discussionmentioning

confidence: 99%

Infusion of UVB-treated splenic stromal cells induces suppression of β cell antigen-specific T cell responses in NOD mice

Xia

Qiu

Peng

et al. 2008

Journal of Autoimmunity

View full text Add to dashboard Cite

Our previous study has demonstrated that transfusion of UVB-irradiation-induced apoptotic β cells effectively prevents type 1 diabetes (T1D) in non-obese diabetic (NOD) mice. However, the limitation of β cell source would preclude the clinical application of this approach. Therefore, in the present study, we have attempted to establish a more practical approach by utilizing apoptotic non-β cells to prevent T1D. We find that apoptotic splenic stromal cells significantly suppress β cell antigen-reactive T cell proliferation in vitro and in vivo. Moreover, β cell antigen-specific T cells primed by β cell antigens in the presence of apoptotic stromal cells have markedly reduced responsiveness to the re-stimulation of the same β cell antigen. We also find that β cell antigenspecific IL-10-producing CD4+ T cells are induced in the presence of apoptotic splenic stromal cells. As expected, transfusion of apoptotic stromal cells effectively protected NOD mice from developing T1D. Furthermore, the proliferation of adoptively transferred β cell antigen-specific TCR-transgenic T cells in pancreatic draining lymph nodes is markedly suppressed in UVB-stroma-treated mice, indicating that UVB-stroma treatment induces immune tolerance to multiple β cell antigens. This study provides an effective and convenient approach for managing T1D by utilizing apoptotic non-β cells.

show abstract

Apoptotic Cells at the Crossroads of Tolerance and Immunity

Cited by 50 publications

References 223 publications

HIV-1 infection–induced apoptotic microparticles inhibit human DCs via CD44

HIV-1 infection–induced apoptotic microparticles inhibit human DCs via CD44

172: Serum endostatin levels are elevated in colorectal cancer and correlate with invasion and systemic inflammatory markers

Infusion of UVB-treated splenic stromal cells induces suppression of β cell antigen-specific T cell responses in NOD mice

Contact Info

Product

Resources

About