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We report for the first time that expression of the novel IL-1 cytokine receptor IL-1Rrp2 (IL-1R6) is unique to DCs within the human myelomonocytic lineage. IL-1Rrp2 was expressed by monocyte-derived dendritic cells (MDDCs) which was dose-dependently increased by IL-4 and correlated with increased numbers of differentiated MDDCs. Human plasmacytoid DCs also express IL-1Rrp2 but the receptor is not expressed by either myeloid DC type 1 (mDC1) or mDC2 cells. We also show that IL-1F8 or IL-1F9 cytokines, which signal through IL-1Rrp2, induce maturation of MDDCs, as measured by increased expression of HLA-DR and CD83 and decreased expression of CD1a. Furthermore, IL-1F8 stimulated increased CD40 and CD80 expression and IL-18 and IL-12 p70 production by MDDCs, which induced proliferation of IFN-γ-producing CD3(+) lymphocytes (indicative of inflammatory Th1 subsets). IL-1F8 and IL-1F2 were equipotent in their ability to stimulate IL-18 secretion from MDDCs but IL-1F8 was not as potent as IL-1F2 in stimulating secretion of IL-12p70 from MDDCs or inducing lymphocyte proliferation Therefore, IL-1Rrp2 expression by some DC subsets may have an important function in the human immune response in vivo via its role in differentiation of inflammatory Th1 lymphocytes. 相似文献
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Mononuclear phagocyte system of human Peyer''s patches: an immunohistochemical study using monoclonal antibodies. 总被引:2,自引:1,他引:2
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Macrophages in sections of human terminal ileal Peyer's patches were studied using a panel of monoclonal antibodies. Germinal centre macrophages were large and strongly positive for acid phosphatase and stained with antibodies RFD1, RFD9, UCHM1 and other macrophage-specific monoclonal antibodies, but not RFD7. In the macrophages of the dome region there was heterogeneity of size and staining for acid phosphatase. The majority of the RFD1 positive cells in this region appeared to be macrophages. However, no RFD9- or RFD7-positive cells were present. By contrast, RFD7-positive but RFD9-negative macrophages were present in the lamina propria. In the interfollicular areas there were cells with a dendritic morphology which were strongly HLA-DR, HLA-DQ and RFD1-positive, but which did not stain with the other macrophage specific monoclonal antibodies or for acid phosphatase. Some macrophages and lymphocytes in the germinal centre and dome regions expressed interleukin 2 and transferrin receptors. These cells were not present in the adjacent lamina propria. 相似文献
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Siddharth Srivastava Ankur Butala Sonal Mahida John Richter Weiyi Mu Hilary Vernon Jay VanGerpen Paldeep S. Atwal Erik H. Middlebrooks David S. Zee SakkuBai Naidu 《American journal of medical genetics. Part A》2019,179(8):1556-1564
Biallelic pathogenic variants in AARS2, a gene encoding the mitochondrial alanyl‐tRNA synthetase, result in a spectrum of findings ranging from infantile cardiomyopathy to adult‐onset progressive leukoencephalopathy. In this article, we present three unrelated individuals with novel compound heterozygous pathogenic AARS2 variants underlying diverse clinical presentations. Patient 1 is a 51‐year‐old man with adult‐onset progressive cognitive, psychiatric, and motor decline and leukodystrophy. Patient 2 is a 34‐year‐old man with childhood‐onset progressive tremor followed by the development of polyneuropathy, ataxia, and mild cognitive and psychiatric decline without leukodystrophy on imaging. Patient 3 is a 57‐year‐old woman with childhood‐onset tremor and nystagmus which preceded dystonia, chorea, ataxia, depression, and cognitive decline marked by cerebellar atrophy and white matter disease. These cases expand the clinical heterogeneity of AARS2‐related disorders, given that the first and third case represent some of the oldest known survivors of this disease, the second is adult‐onset AARS2‐related neurological decline without leukodystrophy, and the third is biallelic AARS2‐related disorder involving a partial gene deletion. 相似文献
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Michael Ian Jarman Kevin Lee Ariel Kanevsky Sarah Min Ilana Schlam Chris Mahida Ali Huda Alexander Milgrom Naila Goldenberg Charles J. Glueck Ping Wang 《BMC blood disorders》2017,17(1):5
Background
Familial and acquired thrombophilia are often etiologic for idiopathic hip and jaw osteonecrosis (ON), and testosterone therapy (TT) can interact with thrombophilia, worsening ON.Case presentation
Case 1: A 62-year-old Caucasian male (previous deep venous thrombosis), on warfarin 1 year for atrial fibrillation (AF), had non-specific right hip-abdominal pain for 2 years. CT scan revealed bilateral femoral head ON without collapse. Coagulation studies revealed Factor V Leiden (FVL) heterozygosity, 4G/4G plasminogen activator inhibitor (PAI) homozygosity, high anti-cardiolipin (ACLA) IgM antibodies, and endothelial nitric oxide (NO) synthase (eNOS) T786C homozygosity (reduced conversion of L-arginine to NO, required for bone health). Apixaban 5 mg twice daily was substituted for warfarin; and L-arginine 9 g/day was started to increase NO. On Apixaban for 8 months, he became asymptomatic. Case 2: A 32-year-old hypogonadal Caucasian male had 10 years of unexplained tooth loss, progressing to primary jaw ON with cavitation 8 months after starting TT gel 50 mg/day. Coagulation studies revealed FVL heterozygosity, PAI 4G/4G homozygosity, and the lupus anticoagulant. TT was discontinued. Jaw pain was sharply reduced within 2 months.Conclusions
Idiopathic ON, often caused by thrombophilia-hypofibrinolysis, is worsened by TT, and its progression may be slowed or stopped by discontinuation of TT and, thereafter, anticoagulation. Recognition of thrombophilia-hypofibrinolysis before joint collapse facilitates anticoagulation which may stop ON, preserving joints.38.
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