Fas Death Receptor Signaling Represses Monocyte Numbers and Macrophage Activation In Vivo.

Brown, Nicholas K.; Hutcheson, Jack; Bickel, Emily; Scatizzi, John C.; Albee, Lee D.; Haines, G. Kenneth; Eslick, Joy; Bradley, Kathleen; Taricone, Elsa; Perlman, Harris

doi:10.4049/jimmunol.174.6.3818-b

Cited by 20 publications

(37 citation statements)

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“…wt and p21 Ϫ/Ϫ mice had equivalent number of leukocytes in peripheral blood (data not shown 26,29,37 As compared to wt mice, p21-deficent mice displayed a marked reduction (3.4-fold; P Ͻ 0.001) in inflammatory monocytes ( Figure 6A). The reduction in inflammatory monocytes was not attributed to increased death, because there was no difference in the percent apoptotic (annexin V-positive) monocytes in peripheral blood (data not shown).…”

Section: P21 ϫ/ϫ Mice Have a Significant Decrease In Inflammatory Monmentioning

confidence: 92%

“…25 Ankle joints were removed and either fixed in 10% neutral buffered formalin for 24 hours and then in ethylenediamine tetraacetic acid-decalcification buffer for 2 weeks, embedded in paraffin, and sectioned or placed in liquid nitrogen, ground into a fine powder by mortal and pestle, digested in protein lysis buffer, and homogenized on ice for 20 seconds. 26 …”

Section: Serum Transfer-induced Arthritismentioning

confidence: 99%

“…Ankles were snap frozen, ground with a mortar and pedestal, and then homogenized in lysis buffer (150 mol/L NaCl, 0.5% Nonidet P-40, 50 mmol/L Tris, 2 mmol/L ethylenediamine tetraacetic acid, pH 8.0, with protease inhibitors and phosphatase inhibitors). 26 All ankle data were normalized by total protein concentration (micrograms/microliter) of the ankle extracts.…”

Section: Enzyme-linked Immunosorbent Assaymentioning

confidence: 99%

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p21Cip1 Is Required for the Development of Monocytes and Their Response to Serum Transfer-induced Arthritis

Scatizzi

Hutcheson

Bickel

et al. 2006

The American Journal of Pathology

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One of the central functions of cyclin-dependent kinase inhibitors, such as p21, p27, or p16, is to prevent entry into the cell cycle. However, the question remains as to whether they have other functions in the cell. We previously demonstrated that overexpression of p21 in fibroblasts isolated from patients with rheumatoid arthritis decreases the production of proinflammatory molecules. Overexpression of p21 has been also shown to reduce the development of experimental arthritis in mice and rats. To explore the role of endogenous p21 in the development of arthritis, we induced arthritis in p21 ؊/؊ mice using the K/BxN serum transfer model of arthritis. Mice deficient in p21 were more resistant to serum transfer-induced arthritis (K/BxN) than wild-type (wt) control mice. Fewer macrophages were detected in p21 ؊/؊ as compared to wt joints following transfer of K/BxN serum. Chemotaxis assays of bone marrow-derived macrophages from p21 ؊/؊ and wt mice revealed no difference in migration. However, there was a substantial decrease in inflammatory monocytes circulating in peripheral blood and in monocyte precursors in bone marrow of p21 ؊/؊ mice as compared to wt mice. Adoptive transfer of wt bone marrow-derived macrophages into p21 ؊/؊ mice restored the sensitivity to serum transfer-induced arthritis. These data suggest a novel role for p21 in regulating the development and/or differentiation of monocytic populations that are crucial for the induction of inflammatory arthritis.

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Section: P21 ϫ/ϫ Mice Have a Significant Decrease In Inflammatory Monmentioning

confidence: 92%

Section: Serum Transfer-induced Arthritismentioning

confidence: 99%

Section: Enzyme-linked Immunosorbent Assaymentioning

confidence: 99%

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p21Cip1 Is Required for the Development of Monocytes and Their Response to Serum Transfer-induced Arthritis

Scatizzi

Hutcheson

Bickel

et al. 2006

The American Journal of Pathology

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“…Unfortunately, effects of increased FasL expression on macrophage capacity to release proinflammatory appear to be variable; in some cases, the spontaneous release of TNF-α is increased by silica (and the subsequent FasL presence; see Borges et al, 2001) while in other studies, the absence of FasL (i.e. demonstrated using lpr/lpr vs. wild-type mice) results in greater spontaneous release of this and other cytokines (Brown et al, 2004) key to inflammation and anti-tumor activities. However, as the overwhelming evidence in the literature supports the former scenario (see reviews by Castranova, 2004 andRimal et al, 2005), and an increased release in cytokines/chemokines would help move the lungs towards a silicotic state, we are left to wonder why these newly-recruited immune cells (macrophages and PMN) would be ineffective against any now-present transformed cells.…”

Section: Disruption Of Tumor Immunity Due To Silicamentioning

confidence: 99%

Dysregulation of the immune system caused by silica and asbestos

Maeda

Nishimura

Kumagai

et al. 2010

Journal of Immunotoxicology

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“…Although CO could modulate CD11b 1 cell expansion in spleen from lupus FcgRIIb KO mice, CO treatment in MRL-Fas lpr lupus mice does not modulate this cell type population. As it has been reported that Fas deficiency plays an active role in different processes, such as keeping circulating monocyte numbers, regulating macrophage activation and migration, it is likely that the lack of Fas provides a more severe impairment in cell regulation than the deficiency of FcgRIIb that cannot be modulated by CO treatment [40]. The fact that CO treatment could not improve MRL-Fas lpr lupus mice survival could be associated with the damage in other tissues, such as in heart and blood vessels, driven by the massive lymphoproliferation [32].…”

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confidence: 99%

Carbon monoxide inhibits T cell activation in target organs during systemic lupus erythematosus

Mackern-Oberti

Obreque

Méndez

et al. 2015

Clinical and Experimental Immunology

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SummarySystemic lupus erythematosus is characterized by the presence of circulating anti-nuclear antibodies (ANA) and systemic damage that includes nephritis, haematological manifestations and pulmonary compromise, among others. Although major progress has been made in elucidating the molecular mechanisms responsible for autoimmunity, current therapies for lupus have not improved considerably. Because the exposure of carbon monoxide (CO) has been shown to display beneficial immunoregulatory properties in different immune-mediated diseases, we investigated whether CO therapy improves lupus-related kidney injury in lupus mice. MRL-Fas lpr lupus mice were exposed to CO and disease progression was evaluated. ANA, leucocyteinfiltrating populations in spleen, kidney and lung and kidney lesions, were measured. CO therapy significantly decreased the frequency of activated B220 1 CD4 2 CD8 2 T cells in kidneys and lungs, as well as serum levels of ANA. Furthermore, we observed that CO therapy reduced kidney injury by decreasing proliferative glomerular damage and immune complexes deposition, decreased proinflammatory cytokine production and finally delayed the impairment of kidney function. CO exposure ameliorates kidney and lung leucocyte infiltration and delays kidney disease in MRLFas lpr lupus mice. Our data support the notion that CO could be explored as a potential new therapy for lupus nephritis.

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Fas Death Receptor Signaling Represses Monocyte Numbers and Macrophage Activation In Vivo.

Cited by 20 publications

References 0 publications

p21Cip1 Is Required for the Development of Monocytes and Their Response to Serum Transfer-induced Arthritis

p21Cip1 Is Required for the Development of Monocytes and Their Response to Serum Transfer-induced Arthritis

Dysregulation of the immune system caused by silica and asbestos

Carbon monoxide inhibits T cell activation in target organs during systemic lupus erythematosus

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