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Titlebook: Immunopathogenetic Mechanisms of Arthritis; J. A. Goodacre,W. Carson Dick Book 1988 MTP Press Limited 1988 genetics.immunity.infection.inf

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书目名称Immunopathogenetic Mechanisms of Arthritis
编辑J. A. Goodacre,W. Carson Dick
视频video
图书封面Titlebook: Immunopathogenetic Mechanisms of Arthritis;  J. A. Goodacre,W. Carson Dick Book 1988 MTP Press Limited 1988 genetics.immunity.infection.inf
描述The fundamental problem facing scientists and clinicians in Rheumatology is that so little is known about the biology of joints. It is our view that a real interface between basic and clinical science offers the best chance of gaining a better understanding of arthritis and in this book we aim to provide a basis for such an interface. Each chapter provides a lucid account of the current literature, reflecting the eminence of each author in their own field. The contributors offer a variety of modern approaches to the study of inflammatory joint disease, illustrating some of the exciting opportunities for research which exist. We hope that those who share our view find these pages informative and stimulating. University of Newcastle upon Tyne, 1987. JOHN A. GOODACRE W. CARSON DICK ix 1 • Polymorphonuclear leukocytes In acute inflammation O. T. G. JONES and A. R. CROSS INTRODUCTION The nonnal function of the professional phagocytes - polymorphonuclear leukocytes (PMN), monocytes, macrophages and eosinophils - is to protect the individual from microbial infection by seeking out and destroying the invading microbes. In order to perform this function effectively the phagocyte must move t
出版日期Book 1988
关键词genetics; immunity; infection; inflammation; macrophages; pathogenesis; pathology
版次1
doihttps://doi.org/10.1007/978-94-009-1293-9
isbn_softcover978-94-010-7075-1
isbn_ebook978-94-009-1293-9
copyrightMTP Press Limited 1988
The information of publication is updating

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Dendritic cells in inflammatory joint disease,ence of cytokines such as interleukin-1 (IL-1). or from the release of degradative enzymes from macrophages. but, whatever the final pathway for destruction of the joint, the underlying activation appears to be immunological. This chapter is not mainly concerned with the afferent or effector mechani
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T-cell activation and function,d modify the immune response. Major recent advances regarding T-cell function and differentiation have led to the definition of unique sub-populations of T lymphocytes by characteristic cell surface glycoproteins (Table 5.1).. Probably the most important breakthrough has resulted in major understand
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Immune reactions in the rheumatoid synovial tissue,ch regulatory and effector mechanisms are involved in the formation of the rheumatic lesions and, most importantly, (ii) what is the specificity (specificities) of the immune reactions responsible for the subsequent development of the multiple immunological and inflammatory events that can be observ
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Experimental animal models of chronic arthritis,mmunological reaction directed at either: (i) an exogenous agent that localizes to the joints or (ii) an articular autoantigen. These concepts, as suggested by studies of arthritis in animals, will almost certainly be modified in the future since immunological reactions directed at exogenous or host
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