Peter E. Lipsky – författare

Targeted therapies of rheumatic diseases have become a reality and have completely changed patient care as well as patient expectations. Initial success with therapies aimed at blocking TNF and IL-1 has stimulated the development of additional targeted approaches focused on other cytokines as well as specific cells and pathways involved in the path

Targeted therapies of rheumatic diseases have become a reality and have completely changed patient care as well as patient expectations. Initial success with therapies aimed at blocking TNF and IL-1 has stimulated the development of additional targeted approaches focused on other cytokines as well as specific cells and pathways involved in the path

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.

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.

The immune system has been known to be capable of distinguishing self from non-self since the pioneering work of Paul Erhlich more than a century ago. Originally described in experiments studying blood transfusion comp- ibility, the principle of “horror autotoxicus” is still valid, although today the phenomenon is usually described in terms of tolerance or ignorance. A great deal has been learned about the various processes preventing self-reactivity normally. These include processes that operate during immune cell ontogeny and subsequently on reactivity of mature lymphocytes in the periphery. They encompass mechanisms that are intrinsic to potentially reactive lymphocytes and can result in central or peripheral deletion or the alteration of functional potential. In addition, there are in?uences that are extrinsic to potentially auto-reactive lymphocytes, including the function of regulatory cells, d- ferentiation state of antigen-presenting cells, availability of self-antigen, the cytokine and chemokine milieu, as well as the traf?cking patterns involved in generating productive immune interactions. It is clear that the immune system devotes a considerable effort to the avoidance of the development of potentially pathogenic self-reactivity. Despite this, the development of self-reactivity is relatively common. - though the development of autoimmune disease is less frequent, autoimmune diseases, such as rheumatoid arthritis, multiple sclerosis, systemic lupus e- thematosus, psoriasis, thyroiditis, and myasthenia gravis, are all too common, and can cause considerable morbidity and even mortality.

The immune system has been known to be capable of distinguishing self from non-self since the pioneering work of Paul Erhlich more than a century ago. Originally described in experiments studying blood transfusion comp- ibility, the principle of “horror autotoxicus” is still valid, although today the phenomenon is usually described in terms of tolerance or ignorance. A great deal has been learned about the various processes preventing self-reactivity normally. These include processes that operate during immune cell ontogeny and subsequently on reactivity of mature lymphocytes in the periphery. They encompass mechanisms that are intrinsic to potentially reactive lymphocytes and can result in central or peripheral deletion or the alteration of functional potential. In addition, there are in?uences that are extrinsic to potentially auto-reactive lymphocytes, including the function of regulatory cells, d- ferentiation state of antigen-presenting cells, availability of self-antigen, the cytokine and chemokine milieu, as well as the traf?cking patterns involved in generating productive immune interactions. It is clear that the immune system devotes a considerable effort to the avoidance of the development of potentially pathogenic self-reactivity. Despite this, the development of self-reactivity is relatively common. - though the development of autoimmune disease is less frequent, autoimmune diseases, such as rheumatoid arthritis, multiple sclerosis, systemic lupus e- thematosus, psoriasis, thyroiditis, and myasthenia gravis, are all too common, and can cause considerable morbidity and even mortality.

The immune system has been known to be capable of distinguishing self from non-self since the pioneering work of Paul Erhlich more than a century ago. Originally described in experiments studying blood transfusion comp- ibility, the principle of “horror autotoxicus” is still valid, although today the phenomenon is usually described in terms of tolerance or ignorance. A great deal has been learned about the various processes preventing self-reactivity normally. These include processes that operate during immune cell ontogeny and subsequently on reactivity of mature lymphocytes in the periphery. They encompass mechanisms that are intrinsic to potentially reactive lymphocytes and can result in central or peripheral deletion or the alteration of functional potential. In addition, there are in?uences that are extrinsic to potentially auto-reactive lymphocytes, including the function of regulatory cells, d- ferentiation state of antigen-presenting cells, availability of self-antigen, the cytokine and chemokine milieu, as well as the traf?cking patterns involved in generating productive immune interactions. It is clear that the immune system devotes a considerable effort to the avoidance of the development of potentially pathogenic self-reactivity. Despite this, the development of self-reactivity is relatively common. - though the development of autoimmune disease is less frequent, autoimmune diseases, such as rheumatoid arthritis, multiple sclerosis, systemic lupus e- thematosus, psoriasis, thyroiditis, and myasthenia gravis, are all too common, and can cause considerable morbidity and even mortality.