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Both acute and chronic inflammatory responses are common features of a variety of pathological conditions. Likewise, allergic inflammation is an important reaction in ailments such as asthma and atopic dermatitis. In all of these conditions, the severity and fidelity of the inflammatory response is dependent on the recruitment of activated inflammatory cells into inflamed sites and on cellular communication. Although this is often achieved through direct cell-to-cell adhesion via specific intercellular adhesion molecules, cells also signal one another using soluble mediators, such as cytokines and chemokines. Moreover, one population of cells may respond directly to a specific stimulus by elaborating a particular cytokine to exert effects on a yet another population of cells; for example, inflammatory effector cells (monocytes and neutrophils) may be locally recruited and activated in response to specific chemotactic signals, resulting in further amplification of a cytokine cascade. Non-immune cells, such as endothelial and epithelial cells and other stromal cells, also play key roles in the generation, maintenance and resolution of both local and systemic inflammatory responses. The thirteen articles in this special issue, entitled “The kinetics and profiles of inflammatory cells during inflammatory and allergic responses,” address the biology and function of various cell populations under both normal and pathophysiological conditions. First discussed are the inflammatory effector cells, including polymorphonuclear neutrophils, which act as a first line of defense, and macrophages, which participate in inflammatory and immunological responses (Chapters 1 and 2). In Chapters 3 and 4, the involvement of T cells in such autoimmune diseases as rheumatoid arthritis and systemic lupus erythematosus is discussed. Recent advances in our understanding of the roles played by cytokines and chemokines during pulmonary diseases are presented in Chapters 5 and 7, while the role of bronchial epithelial cells in allergic reactions is discussed in Chapter 6. The importance of endothelial cells in both angiogenesis and inflammation is now well recognized. Chapter 8 summarizes the most relevant information on adhesion molecules and anti-adhesive and anti-angiogenic agents. In Chapter 9, the authors review recent findings on the role of osteoclasts and osteoblasts in bone remodeling under normal conditions and such pathophysiological conditions as rheumatoid arthritis. Dysregulation of inflammatory mediators or their receptors in keratinocytes during the evolution of chronic inflammatory skin diseases is discussed in Chapter 10. In Chapter 11, the authors review recent findings indicating that the reciprocal interaction of activated glial cells, COX enzymes and prostaglandins mediate both neurodegeneration and neuroprotection during brain inflammation. Finally, the crucial role played by renal mesangial and epithelial cells in the glomerular injury and inflammation seen in such ailments as glomerulonephritis are discussed in Chapters 12 and 13. I hope that this special issue sheds light on all the major cell populations involved in acute and chronic inflammation and in aberrant immune responses. Our increased understanding of the roles of specific cell types, cell surface molecules and their products at inflamed sites may provide the basis for new approaches to therapeutic immunointervention in disease processes. More broadly, it should contribute to our understanding of the pathobiological mechanisms of a variety of diseases affecting every organ system.