The Experts below are selected from a list of 48 Experts worldwide ranked by ideXlab platform
Julien Y. Bertrand - One of the best experts on this subject based on the ideXlab platform.
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Yolk sac hematopoiesis: does it contribute to the adult hematopoietic system?
Cellular and Molecular Life Sciences, 2020Co-Authors: Valerie Wittamer, Julien Y. BertrandAbstract:In most vertebrates, the yolk sac (YS) represents the very first Tissue where blood cells are detected. Therefore, it was thought for a long time that it generated all the blood cells present in the embryo. This model was challenged using different animal models, and we now know that YS hematopoietic precursors are mostly transient although their contribution to the adult system cannot be excluded. In this review, we aim at properly define the different waves of blood progenitors that are produced by the YS and address the fate of each of them. Indeed, in the last decade, many evidences have emphasized the role of the YS in the emergence of several Myeloid Tissue-resident adult subsets. We will focus on the development of microglia, the resident macrophages in the central nervous system, and try to untangle the recent controversy about their origin.
Valerie Wittamer - One of the best experts on this subject based on the ideXlab platform.
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Yolk sac hematopoiesis: does it contribute to the adult hematopoietic system?
Cellular and Molecular Life Sciences, 2020Co-Authors: Valerie Wittamer, Julien Y. BertrandAbstract:In most vertebrates, the yolk sac (YS) represents the very first Tissue where blood cells are detected. Therefore, it was thought for a long time that it generated all the blood cells present in the embryo. This model was challenged using different animal models, and we now know that YS hematopoietic precursors are mostly transient although their contribution to the adult system cannot be excluded. In this review, we aim at properly define the different waves of blood progenitors that are produced by the YS and address the fate of each of them. Indeed, in the last decade, many evidences have emphasized the role of the YS in the emergence of several Myeloid Tissue-resident adult subsets. We will focus on the development of microglia, the resident macrophages in the central nervous system, and try to untangle the recent controversy about their origin.
Daniel G Remick - One of the best experts on this subject based on the ideXlab platform.
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a2b adenosine receptor expression by Myeloid cells is proinflammatory in murine allergic airway inflammation
Journal of Immunology, 2012Co-Authors: Bryan Belikoff, Louis J Vaickus, Michail V Sitkovsky, Daniel G RemickAbstract:Asthma is a chronic condition with high morbidity and healthcare costs, and cockroach allergens are an established cause of urban pediatric asthma. A better understanding of cell types involved in promoting lung inflammation could provide new targets for the treatment of chronic pulmonary disease. Because of its role in regulating Myeloid cell-dependent inflammatory processes, we examined A 2B R expression by Myeloid cells in a cockroach allergen model of murine asthma-like pulmonary inflammation. Both systemic and Myeloid Tissue-specific A 2B R deletion significantly decreased pulmonary inflammatory cell recruitment, airway mucin production, and proinflammatory cytokine secretion after final allergen challenge in sensitized mice. A 2B R deficiency resulted in a dramatic reduction on Th2-type airways responses with decreased pulmonary eosinophilia without augmenting neutrophilia, and decreased lung IL-4, IL-5, and IL-13 production. Chemokine analysis demonstrated that eotaxin 1 and 2 secretion in response to repeated allergen challenge is Myeloid cell A 2B R dependent. In contrast, there were no differences in the levels of the CXC chemokines keratinocyte-derived chemokine and MIP-2 in the Myeloid cell A 2B R-deficient mice, strengthening A 2B R involvement in the development of Th2-type airways inflammation. Proinflammatory TNF-α, IFN-γ, and IL-17 secretion were also reduced in systemic and Myeloid Tissue-specific A 2B R deletion mouse lines. Our results demonstrate Th2-type predominance for A 2B R expression by Myeloid cells as a mechanism of development of asthma-like pulmonary inflammation.
David Taieb - One of the best experts on this subject based on the ideXlab platform.
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adrenal myelolipoma an unusual cause of bilateral highly 18f fdg avid adrenal masses
The Journal of Clinical Endocrinology and Metabolism, 2012Co-Authors: Frederic Castinetti, A Verschueren, P Cassagneau, Thierry Brue, Frederic Sebag, L Daniel, David TaiebAbstract:A 77-yr-old man presented with rapidly progressive cerebellar syndrome,extrapyramidal signs,andcognitive impairment. Past medical history reported a prostate cancer treated by external radiotherapy and an essential thrombocytemia with sideroblastic anemia. Brain computed tomography (CT) scan was normal. The combination of positive antineutrophil antibodies and brain 18F-fluorodeoxyglucose (18F-FDG) positron emission tomography (PET) uptake pattern was suggestive of paraneoplastic neurological syndrome. Whole-body PET imaging revealed bilateral hypermetabolic adrenal masses (right and left adrenal maximumstandardizeduptakevalue 11.4and8.0).Abdominal CTscanshowedbilateralheterogeneousadrenalmassescontaining soft Tissue and adipose components (Fig. 1). Complete endocrinological workup (24-h urinary free cortisol, low-dose dexamethasone suppression test, plasma aldosterone level, dehydroepiandrosterone sulfate, and urinary and plasma methoxyamines) was normal. A CT scan-guided adrenal puncture was performed to rule out malignancy. Pathological analyses were concordant with the diagnosis of myelolipoma. Bilateral high 18F-FDG PET uptake is usually due to adrenal malignancies (i.e. metastases, primary adrenal lymphoma) (1). A recent study has also reported an intense glucose hypermetabolism in bilateral adrenal hyperplasia with Cushing’s syndrome, which was not observed in our patient (2).Wereporthereavery rare caseofbenignhypermetabolic masses secondary to adrenal myelolipomas. The few reported cases of adrenal myelolipoma have usually shown no significant 18F-FDG uptake. An unusual case of giant adrenal myelolipoma with increased 18F-FDG uptake has been reported (3). In another case, high tracer avidity was due to a lung cancer metastasis within a myelolipoma (4). Interestingly, in our case, increased 18F-FDG avidity could be explained by overexpression of glucose transporter-1 within the Myeloid Tissue component of the mass (5). Myelolipomas should be considered as potential differential diagnoses of high 18F-FDG avid adrenal lesions, which consequently do not necessarily require adrenalectomy. A CT-guided biopsy directed at the focal area of hypermetabolism may be needed to rule out malignancy.
Bryan Belikoff - One of the best experts on this subject based on the ideXlab platform.
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a2b adenosine receptor expression by Myeloid cells is proinflammatory in murine allergic airway inflammation
Journal of Immunology, 2012Co-Authors: Bryan Belikoff, Louis J Vaickus, Michail V Sitkovsky, Daniel G RemickAbstract:Asthma is a chronic condition with high morbidity and healthcare costs, and cockroach allergens are an established cause of urban pediatric asthma. A better understanding of cell types involved in promoting lung inflammation could provide new targets for the treatment of chronic pulmonary disease. Because of its role in regulating Myeloid cell-dependent inflammatory processes, we examined A 2B R expression by Myeloid cells in a cockroach allergen model of murine asthma-like pulmonary inflammation. Both systemic and Myeloid Tissue-specific A 2B R deletion significantly decreased pulmonary inflammatory cell recruitment, airway mucin production, and proinflammatory cytokine secretion after final allergen challenge in sensitized mice. A 2B R deficiency resulted in a dramatic reduction on Th2-type airways responses with decreased pulmonary eosinophilia without augmenting neutrophilia, and decreased lung IL-4, IL-5, and IL-13 production. Chemokine analysis demonstrated that eotaxin 1 and 2 secretion in response to repeated allergen challenge is Myeloid cell A 2B R dependent. In contrast, there were no differences in the levels of the CXC chemokines keratinocyte-derived chemokine and MIP-2 in the Myeloid cell A 2B R-deficient mice, strengthening A 2B R involvement in the development of Th2-type airways inflammation. Proinflammatory TNF-α, IFN-γ, and IL-17 secretion were also reduced in systemic and Myeloid Tissue-specific A 2B R deletion mouse lines. Our results demonstrate Th2-type predominance for A 2B R expression by Myeloid cells as a mechanism of development of asthma-like pulmonary inflammation.
