Titlebook: Chemokines in Disease; Biology and Clinical Caroline A. Hébert (Senior Scientist) Book 1999 Springer Science+Business Media New York 1999 C

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The Role of Chemokines in Allergic Airway Inflammationsease likely reflect the lack of our understanding of the mechanisms that cause airway inflammation and hyperreactivity. The major pathophysiological event that occurs during asthma is airway hyperreactivity during the late-phase response. The initial induction of IgE-mediated mast cell degranulatio

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The Role of CC Chemokines in Th1- and Th2-Type Pulmonary Inflammation Modelsalveolar macrophages and mast cells) and nonimmune (i.e., epithelial) cells. These mediators modulate the function of these cells and also promote the infiltration of lymphocytes and phagocytes, and the concerted efforts of all of these cells facilitate the destruction and/or clearance of the inflam

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The Role of ELR+-CXC Chemokines in Wound Healing and Melanoma Biologytif at the amino terminus are angiogenic (.), whereas those not containing this motif are angiostatic (.) .. The murine . orthologs are . and .-2. The chemokine-β subfamily, noted by two adjacent cysteines (CC) at the N terminus, includes RANTES, MCP-1-3, MIP-1α and β, and numerous others .. Only on

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Engineering, Biology, and Clinical Development of hMIP-1αation into more committed progenitors .. Therefore, once dividing, their survival is in jeopardy during cytotoxic drug therapy and a specific inhibitor of stem cell division might be expected to find use as an adjunct to chemotherapy. In clinical oncology, the expectation would be that stem-cell pro

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M. Trzciński,T. S. Kavetskyy,A. L. Stepanovm lies in the realm of host defense. However, the obviously critical role of several alpha chemokines and their receptors in developmental biology may lead to other interpretations, as will be discussed in a following section.

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https://doi.org/10.1007/978-3-319-75118-4sease likely reflect the lack of our understanding of the mechanisms that cause airway inflammation and hyperreactivity. The major pathophysiological event that occurs during asthma is airway hyperreactivity during the late-phase response. The initial induction of IgE-mediated mast cell degranulatio