Regulation of Immune Response and Inflammatory Reactions against Viral Infection by VCAM-1

Ou, Rong; Zhang, Menghua; Huang, Lei; Flavell, Richard A.; Koni, Pandelakis A.; Moskophidis, Demetrius

doi:10.1128/jvi.02191-07

Cited by 28 publications

(28 citation statements)

References 73 publications

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“…Indeed, a CD8-T cell-mediated pathologic cascade triggered by DC presentation can be lethal to mice during LCMV infection 35 . We postulate that the absence of miR-22 may cause defective APC cross activation of T cells in response to infection, which may have contributed to the improved survival of miR-22 KO mice compared to WT.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-22 controls interferon alpha production and erythroid maturation in response to infectious stress in mice

Kadmon

Landers

et al. 2017

Experimental Hematology

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MicroRNA-22 (miR-22) is a highly conserved microRNA that can regulate cell proliferation, oncogenesis, and cell maturation, especially during stress. In hematopoietic stem cells (HSCs) miR-22 has been reported to be involved in the regulation of key self-renewal factors including Tet2. Recent work demonstrates that miR-22 also participates in regulation of the interferon response, and expression profiling studies suggest that it is variably expressed at different stages in erythroid differentiation. We thus hypothesized that miR-22 regulates maturation of erythroid progenitors during stress hematopoiesis through its interaction with interferon. We compared the blood and bone marrow of wild type (WT) and miR-22-deficient mice at baseline and upon infectious challenge with systemic lymphochoriomeningitis (LCMV) virus. MiR-22-deficient mice maintained platelet counts better than WT mice during infection, but they showed significantly reduced red blood cells (RBC) and hemoglobin. Analysis of bone marrow progenitors demonstrated better overall survival and improved HSC homeostasis in infected miR-22-null mice compared to WT, attributable to a blunted interferon response to LCMV challenge in the miR-22-null mice. We found that miR-22 was exclusively expressed in stage II erythroid precursors and was downregulated upon infection in WT mice. Our results indicate that miR-22 promotes the interferon response to viral infection and that it functions at baseline as a brake to slow erythroid differentiation and maintain adequate erythroid potential. Impaired regulation of erythrogenesis in the absence of miR-22 can lead to anemia during infection.

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Section: Discussionmentioning

confidence: 99%

MicroRNA-22 controls interferon alpha production and erythroid maturation in response to infectious stress in mice

Kadmon

Landers

et al. 2017

Experimental Hematology

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“…Immune cells such as monocytes, macrophages, dendritic cells and lymphocytes migrate into atherosclerotic lesions, to contribute to inflammation by interacting with other proinflammatory immune cells [16]–[19]. Activated immune cells secrete a range of pro-inflammatory cytokines to intensify the inflammatory process locally.…”

Section: Discussionmentioning

confidence: 99%

Depletion of B2 but Not B1a B Cells in BAFF Receptor-Deficient ApoE−/− Mice Attenuates Atherosclerosis by Potently Ameliorating Arterial Inflammation

et al. 2012

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We have recently identified conventional B2 cells as atherogenic and B1a cells as atheroprotective in hypercholesterolemic ApoE−/− mice. Here, we examined the development of atherosclerosis in BAFF-R deficient ApoE−/− mice because B2 cells but not B1a cells are selectively depleted in BAFF-R deficient mice. We fed BAFF-R−/− ApoE−/− (BaffR.ApoE DKO) and BAFF-R+/+ApoE−/− (ApoE KO) mice a high fat diet (HFD) for 8-weeks. B2 cells were significantly reduced by 82%, 81%, 94%, 72% in blood, peritoneal fluid, spleen and peripheral lymph nodes respectively; while B1a cells and non-B lymphocytes were unaffected. Aortic atherosclerotic lesions assessed by oil red-O stained-lipid accumulation and CD68+ macrophage accumulation were decreased by 44% and 50% respectively. B cells were absent in atherosclerotic lesions of BaffR.ApoE DKO mice as were IgG1 and IgG2a immunoglobulins produced by B2 cells, despite low but measurable numbers of B2 cells and IgG1 and IgG2a immunoglobulin concentrations in plasma. Plasma IgM and IgM deposits in atherosclerotic lesions were also reduced. BAFF-R deficiency in ApoE−/− mice was also associated with a reduced expression of VCAM-1 and fewer macrophages, dendritic cells, CD4+ and CD8+ T cell infiltrates and PCNA+ cells in lesions. The expression of proinflammatory cytokines, TNF-α, IL1-β and proinflammatory chemokine MCP-1 was also reduced. Body weight and plasma cholesterols were unaffected in BaffR.ApoE DKO mice. Our data indicate that B2 cells are important contributors to the development of atherosclerosis and that targeting the BAFF-R to specifically reduce atherogenic B2 cell numbers while preserving atheroprotective B1a cell numbers may be a potential therapeutic strategy to reduce atherosclerosis by potently reducing arterial inflammation.

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“…In clinical trials, blocking the VCAM-1 ligand, α4-integrin, with antibodies (natalizumab) reduces disease severity in multiple sclerosis and Crohn’s disease [65, 66]. VCAM-1 also has a role in regulation of infection because during lymphocytic choriomeningitis virus (LCMV) infections, VCAM-1 on the endothelium mediates CD8+ T cell, monocyte and dendritic cell infiltration into the brain [67]. In experimental visceral leishmaniasis, VCAM-1 interaction with α4β1 integrin regulates the production of dendritic cells since antibody inhibition of VCAM-1 or α4β1-integrin blocks the dendritic cell response in the spleens in these mice [68].…”

Section: Vcam-1 Function In Disease and Infectionsmentioning

confidence: 99%

Isoforms of Vitamin E Differentially Regulate Inflammation

Cook‐Mills¹,

McCary²

2010

EMIDDT

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Vitamin E regulation of disease has been extensively studied in humans, animal models and cell systems. Most of these studies focus on the α-tocopherol isoform of vitamin E. These reports indicate contradictory outcomes for anti-inflammatory functions of the α-tocopherol isoform of vitamin E, especially with regards to clinical studies of asthma and atherosclerosis. These seemingly disparate clinical results are consistent with recently reported unrecognized properties of isoforms of vitamin E. Recently, it has been reported that physiological levels of purified natural forms of vitamin E have opposing regulatory functions during inflammation. These opposing regulatory functions by physiological levels of vitamin E isoforms impact interpretations of previous studies on vitamin E. Moreover, additional recent studies also indicate that the effects of vitamin E isoforms on inflammation are only partially reversible using physiological levels of a vitamin E isoform with opposing immunoregulatory function. Thus, this further influences interpretations of previous studies with vitamin E in which there was inflammation and substantial vitamin E isoforms present before the initiation of the study. In summary, this review will discuss regulation of inflammation by vitamin E, including alternative interpretations of previous studies in the literature with regards to vitamin E isoforms.

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Regulation of Immune Response and Inflammatory Reactions against Viral Infection by VCAM-1

Cited by 28 publications

References 73 publications

MicroRNA-22 controls interferon alpha production and erythroid maturation in response to infectious stress in mice

MicroRNA-22 controls interferon alpha production and erythroid maturation in response to infectious stress in mice

Depletion of B2 but Not B1a B Cells in BAFF Receptor-Deficient ApoE−/− Mice Attenuates Atherosclerosis by Potently Ameliorating Arterial Inflammation

Isoforms of Vitamin E Differentially Regulate Inflammation

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