Restoration of C1q levels by bone marrow transplantation attenuates autoimmune disease associated with C1q deficiency in mice

Cortés-Hernández, Josefina; Fossati-Jimack, Liliane; Petry, Franz; Loos, Michael; Izui, Shozo; Walport, Mark J.; Cook, H. Terence; Botto, Marina

doi:10.1002/eji.200425616

Cited by 46 publications

(28 citation statements)

References 39 publications

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“…At the age of 14 months some MRL/MpJ +/+ mice exhibited GN with increased glomerular cellularity as well as glomerular IgG, C1q and/or C3 deposition. This is in accordance with previous studies showing glomerular deposition of C3 and IgG starting already at 7 months [11,17].…”

Section: Discussionsupporting

confidence: 94%

Anti-C1q autoantibodies do not correlate with the occurrence or severity of experimental lupus nephritis

Bigler

Hopfer

Danner

et al. 2010

Molecular Immunology

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Section: Discussionsupporting

confidence: 94%

Anti-C1q autoantibodies do not correlate with the occurrence or severity of experimental lupus nephritis

Bigler

Hopfer

Danner

et al. 2010

Molecular Immunology

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“…Many investigators have reported that impaired clearance of dying cells plays a pathogenic role in the development of autoimmunity (57)(58)(59)(60). Moreover, it has been reported that macrophages of autoimmune-prone mice, such as MRL/Mp or NOD mice, showed reduced phagocytosis of apoptotic cells (61)(62)(63)(64)(65).…”

Section: Discussionmentioning

confidence: 99%

Neutrophils Accelerate Macrophage-Mediated Digestion of Apoptotic Cells In Vivo as Well as In Vitro

Iyoda

Nagata

Akashi³

et al. 2005

The Journal of Immunology

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It is generally believed that the clearance of apoptotic cells does not lead to inflammation. In contrast, we previously found that injection of apoptotic cells into the peritoneal cavity induced the expression of an inflammatory chemokine, MIP-2, and infiltration of neutrophils, and that anti-MIP-2 Abs suppressed the infiltration significantly. Because our previous study showed that whole-body x-irradiation caused neutrophil infiltration into the thymus along with T cell apoptosis, we examined the role of neutrophils in apoptotic cell clearance. Neutrophil infiltration reached a peak 12 h after irradiation with 1 Gy of x-rays. Immunohistological analysis revealed that apoptotic cells disappeared dramatically from 10.5 to 12 h after x-irradiation. As neutrophils moved from an inner area of the cortex to the periphery, apoptotic cells disappeared concomitantly. Either anti-MIP-2 or anti-CXCR2 Abs suppressed neutrophil infiltration significantly, and the suppression of neutrophil infiltration by anti-MIP-2 Abs delayed the disappearance of apoptotic cells. Moreover, macrophage-mediated digestion of apoptotic thymocytes was accelerated in vitro on coculturing with neutrophils, even if neutrophils were separated from macrophages. These results suggest that neutrophils are recruited to the thymus mainly by MIP-2 after whole-body x-irradiation and that such neutrophils may not induce inflammation but rather accelerate complete digestion of apoptotic cells by macrophages.

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“…This result was anticipated (4, 7) due to the multifactorial nature of lupus. Indeed, genetic background is a determining factor for lupus disease development in mice with mutations for lupusrelated genes (36,37); thus, whereas lack of Fas leads to fullblown lupus in combination with the MRL background, it causes milder disease in C57BL/6 mice (38).…”

Section: Discussionmentioning

confidence: 99%

p21CIP1/WAF1 Controls Proliferation of Activated/Memory T Cells and Affects Homeostasis and Memory T Cell Responses

Arias

Ballesteros-Tato

García

et al. 2007

The Journal of Immunology

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Development of autoantibodies and lupus-like autoimmunity by 129/Sv × C57BL/6 p21−/− mice has established that cell cycle deregulation is one the defective pathways leading to break of tolerance. Memory T cell accumulation is thought to be related to tolerance loss in murine lupus models. We studied T cell memory responses in C57BL/6 p21−/− mice that develop lupus-like disease manifestations. p21 did not affect primary proliferation of naive T cells, and was required for cycling control, but not for apoptosis of activated/memory T cells. When we induced apoptosis by secondary TCR challenge, surviving memory T cells depended on p21 for proliferation control. Under conditions of secondary T cell stimulation that did not cause apoptosis, p21 was also needed for regulation of activated/memory T cell expansion. The requirement for p21 in the control of T cell proliferation of activated/memory T cells suggests that in addition to apoptosis, cycling regulation by p21 constitutes a new pathway for T cell homeostasis. Concurring with this view, we found accumulation in p21−/− mice of memory CD4+ T cells that showed increased proliferative potential after TCR stimulation. Furthermore, OVA immunization of p21−/− mice generated hyperresponsive OVA-specific T cells. Overall, the data show that p21 controls the proliferation of only activated/memory T cells, and suggest that p21 forms part of the memory T cell homeostasis mechanism, contributing to maintenance of tolerance.

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Restoration of C1q levels by bone marrow transplantation attenuates autoimmune disease associated with C1q deficiency in mice

Cited by 46 publications

References 39 publications

Anti-C1q autoantibodies do not correlate with the occurrence or severity of experimental lupus nephritis

Anti-C1q autoantibodies do not correlate with the occurrence or severity of experimental lupus nephritis

Neutrophils Accelerate Macrophage-Mediated Digestion of Apoptotic Cells In Vivo as Well as In Vitro

p21CIP1/WAF1 Controls Proliferation of Activated/Memory T Cells and Affects Homeostasis and Memory T Cell Responses

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