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Most lymphocytes recirculate throughout the body, migrating from blood through organized lymphoid tissues such as lymph nodes (LN) and Peyer's patches (PP), then to lymph and back to blood (GOWANS and KNIGHT 1964). Smaller numbers of lymphocytes migrate from blood to extranodal tissues such as pancreas and then through lymphatic vessels to LN (MACKAY et al. 1990). An important feature of this migration is the ability of lymphocytes to recognize and adhere to the surface of blood vessel endothelial cells before migrating through the vessel wall into surrounding tissue (CARLOS and HARLAN 1994; IMHOF and DUNON 1995; BUTCHER and PICKER 1996). Adhesion interactions of vascular endothelium with lymphocytes under flow or shear consist of at least four steps: (I) an initial transient sticking or rolling; (2) if the lymphocytes encounter appropriate activating or chemotactic factors in the local environment, rolling may be followed by a lymphocyte activation step that then leads to; (3) strong adhesion or sticking that may be followed by; (4) lym phocyte diapedesis into tissue (BUTCHER 1991; SHIMUZU et al. 1992; SPRINGER 1994; BARGATZE et al. 1995). Specific lymphocyte and endothelial adhesion molecules (AM) are involved in each step of this "adhesion cascade" (reviewed in CARLOS and HARLAN 1994; IMHOF and DUNON 1995; BUTCHER and PICKER 1996). This allows lymphocyte migration to be controlled at several different steps, leading to a combinatorial increase in specificity and sensitivity.
The microcirculation is highly responsive to, and a vital participant in, the inflammatory response. All segments of the microvasculature (arterioles, capillaries, and venules) exhibit characteristic phenotypic changes during inflammation that appear to be directed toward enhancing the delivery of inflammatory cells to the injured/infected tissue, isolating the region from healthy tissue and the systemic circulation, and setting the stage for tissue repair and regeneration. The best characterized responses of the microcirculation to inflammation include impaired vasomotor function, reduced capillary perfusion, adhesion of leukocytes and platelets, activation of the coagulation cascade, and enhanced thrombosis, increased vascular permeability, and an increase in the rate of proliferation of blood and lymphatic vessels. A variety of cells that normally circulate in blood (leukocytes, platelets) or reside within the vessel wall (endothelial cells, pericytes) or in the perivascular space (mast cells, macrophages) are activated in response to inflammation. The activation products and chemical mediators released from these cells act through different well-characterized signaling pathways to induce the phenotypic changes in microvessel function that accompany inflammation. Drugs that target a specific microvascular response to inflammation, such as leukocyte-endothelial cell adhesion or angiogenesis, have shown promise in both the preclinical and clinical studies of inflammatory disease. Future research efforts in this area will likely identify new avenues for therapeutic intervention in inflammation. Table of Contents: Introduction / Historical Perspectives / Anatomical Considerations / Impaired Vasomotor Responses / Capillary Perfusion / Angiogenesis / Leukocyte-Endothelial Cell Adhesion / Platelet-Vessel Wall Interactions / Coagulation and Thrombosis / Endothelial Barrier Dysfunction / Epilogue / References
Integrins: Molecular and Biological Responses to the Extracellular Matrix will help basic, applied, and clinical researchers keep up with the explosion of literature on the integrin family of proteins. This volume extends material previously covered in Receptors for Extracellular Matrix. It addresses some of the most exciting areas of integrin biology, including the varied roles of integrins in cell division, differentiation, movement, wound healing, inflammation, thrombosis, osteoporosis, and cancer. Describes key aspects of integrin structure, function, and biology Covers collagen receptors, epithelial cell integrins, leukocyte integrins, platelet integrins, integrin signaling, and integrin antagonists Investigates the expression and role of integrins during development and in the cytoskeleton Includes the actions and influences of integrins in inflammation, thrombosis, and osteoporosis
This volume of Current Topics in Microbiology and Immunology was planned in parallel with an EM BO workshop on cell-cell Interactions in Leukocyte Homing and Differentiation held at the Basel Institute for Immunology in November 1992, and many of the workshop speakers have contributed to it. Cell adhesion is one of the most dynamic fields of biological research and presented in this book is the current knowledge on the structure and function of the major families of cell adhesion molecules-the integrins, the selectins, the immunoglobulin superfamily, and CD44. Complex interactions between the members of these families mediate diverse adhesion functions, including leukocyte-leukocyte interactions, lymphocyte homing, inflammation, and lymphocyte-stromal cell interaction during hematopoiesis. A great deal of emphasis is placed on the regulatory elements that control the expression and function of adhesion molecules. Cytokines not only induce the expression of certain adhesion molecules, but may also modify their functional status. For instance, the integrins exist in either an inactive nonfunctional form or an active functional form, and a number of intracellular or extracellular stimuli modify integrin function. This is particularly important during leukocyte binding to endothelium and transendothelial migration, which proceeds through a cascade of adhesion events. Although cell adhesion molecules play an important role in many processes, this book concentrates on their role within the immune system. A number of chapters discuss the migration of lymphocytes between hematopoietic organs such as the thymus, lymph nodes, Peyer's patches, and spleen.
Leukocyte adhesion molecules have been the subject of intense basic and preclinical research. Results from clinical trials obtained sofar with antibodies directed towards these surface proteins offer promise for the prevention of graft rejection and effective treatment of acute and chronic inflammatory disease. This volume presents a comprehensive review of contemporary research on the structure, function and regulation of leukocyte adhesion molecules and their ligands, from the molecular to the clinical level. The blend of basic science and clinical applications presented in Structure, Function and Regulation of Molecules Involved in Leukocyte Adhesion provides clear evidence of the biological importance of cell-cell interactions and the many potential clinical dividends afforded by understanding the molecular basis of cell adhesion. It will appeal to a broad range of readers in immunology and cell biology.
This book presents a case history of a patient with leukocyte adhesion deficiency to illustrate essential points about the mechanisms of immunity and to explain some of the immunological problems often seen in the clinic. It is helpful for medical and pre-medical students.
Inflammatory cell recruitment requires the concerted action of at least five major sets of adhesion molecules: integrins, immunoglobulin-like molecules, selectins, carbohydrate structures serving as selectin ligands, and certain ectoenzymes. This volume gives a comprehensive overview on the most relevant leukocyte and endothelial adhesion molecules. The chapters are written by leaders in the field and focus on the biology, structure, function, and regulation of adhesion molecules. Currently approved adhesion molecule-based therapies are reviewed and an outlook for future approaches is also provided. The book is of interest to clinicians and scientists from immunology, physiology, cancer research, rheumatology, allergology, infectious diseases, gastroenterology, pulmonology and cardiology.
Leukocyte adhesion molecules promise to be highly effective as antigens in the antibody-directed leucocyte elimination treatment prior to grafting or in cases of acute and chronic inflammatory disease. This comprehensive review of contemporary research provides thorough discussions of the structure of these molecules, their in vitro function, and the role that they play in vivo as evidenced by results shown in inflammatory models where antibodies against these molecules are given to inhibit their function. The blend of basic science and clinical applications provides clear evidence of the biological relevance of cell-cell interactions and the many potential clinical dividends afforded by understanding the molecular basis of cell adhesion.
The integrin family is composed of 24 members and approximately ten years ago (2003) we published a book devoted to the nine I domain integrin subunits. In this second edition, I am pleased that most of the original authors have been able to contribute to the updated version. I domain containing integrins include collagen receptors and leukocyte receptors. In 2003 the knockout mouse phenotypes for all of the I domain integrins had not yet been published; they are now, and are summarized and discussed in this edition. Interestingly, a recent 10 integrin mutation in dogs has indicated that collagen-binding integrins in the musculoskeletal system might have much more severe phenotypes in larger animals/humans compared to the mild integrin phenotypes observed in collagen-binding integrin deficient mice. This finding is further discussed in the book. In the cancer field, the microenvironment is taking center stage, and here collagen receptors on fibroblasts are predicted to play important roles in paracrine signaling, in regulating tissue stiffness and matrix remodeling. New technologies, new mouse models in combination with analyses of I integrins in larger animals/humans are thus predicted to increase our knowledge about this group of receptors. With this in mind we look forward to another 10 years of research with I domain integrins.