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Cutaneous T-cell lymphomas (CTCLs) are a heterogeneous group of Non-Hodgkin lymphomas with a variety of clinical presentation and outcomes. The diagnosis and treatment of CTCLs have evolved significantly with advances in our understanding of their pathogenesis and biological behaviors through immunophenotypic, molecular, and cytogenetic analysis and clinical correlation. The diagnosis and classification of CTCLs depend on integration of clinical presentation, histology, immunophenotype, molecular and/or cytogenetic findings. Accurate diagnosis and staging are essential for proper treatment and prognosis of the patients. The book Cutaneous T-Cell Lymphoma (CTCL): Clinical Features, Diagnosis and Treatment Options aims to provide the most up-to-date knowledge of the diagnosis, prognosis and treatment strategies of CTCL. Each chapter focuses on a different aspect of CTCL: clinical presentation, pathology, therapeutic options, role of radiation therapy, and in-depth discussion of the specific subtypes of CTCL classified under the most recent World Health Organization (WHO) classification of lymphoid neoplasms. The authors are practicing physicians in major medical centers and university hospitals, and are familiar with the challenges of diagnosing and treating patients with CTCL. The book is written for the practicing physicians and provides practical information and advice for their daily practice. Residents, fellows and other trainees will also find the contents of this book useful for their education and board preparation. The authors hope that the material covered in this book will serve as a foundation for the readers to keep up with future developments in the field.

Our motivation for putting together this book was the need for a single source reference that could be used as an introduction to cell-mediated cytotoxicity for newcomers to this field, such as students and fellows beginning work in our laboratories. At present no such book is available, and we felt that it would be useful as a teaching tool and as a way of conveying our enthusiasm about recent progress in the cytotoxicity field to our colleagues in allied areas. It was with some hesitation that we approached our colleagues with the proposal for this book, and we were pleased to find them very supportive of the idea and willing to participate. We thought it important to broaden the scope of the book to include historical, molecular, cell biological, and clinical aspects of cell-mediated cytotoxicity. To our knowledge this is the first book on cell-mediated cytotoxicity with such a broad scope. Historically, studies on cellular cytotoxicity were part of cellular immunology from its origin. One development of tremendous import was the advent of the 51 Cr assay, which allowed this arm of the immune response to be measured easily and quantitatively. Thus, a readout of this effector pathway is available within a few hours; other immune effector functions can take days or even longer to assay, and the assays are often less quantitative.

The IL-17 cytokines represent a novel family of cytokines, which defines a new effector T cell, the Th17 cell, and extend the Th1-Th2 paradigm. Th17 cells in part co-express at least IL-17A and IL-17F, IL-21 and IL-22. IL-17 A/F are produced by T cells ( and), iNKT cells, and possibly neutrophils, dendritic cells and Paneth cells. The regulation of IL-17 family member's expression, and the identification of effector mechanisms are an area of intense current research. Recognized regulators of IL-17A expression include the nuclear receptor ROR t, proinflammatory cyt- ines such as IL-1, IL-6 with TGF-, IL-21, IL-23 IL-25 in the absence of IFN- and IL-4, which are discussed. Recent data suggest that IL-17A may have a dual fu- tion – pro-inflammatory and anti-inflammatory- suggesting that IL-17A may also contribute to terminate inflammation. Further, a reciprocal regulation of Th17 and regulatory T cells including the role of retinoic acid and TGF- is discussed. The discovery that patients with rheumatoid arthritis, allergic disorders, psor- sis and inflammatory bowel disease express IL-17A generated interest in the medical community and instigated a flurry of experimental research on the potential role of Th17 in inflammatory diseases. Experimental studies confirmed that IL-17A is induced and is critical for the development of allergic lung inflammation, arthritis, bacterial sepsis, experimental allergic encephalomyelitis and myocarditis, as well as other inflammatory con- tions including organ transplantation. The role of IL-17F and IL-22 is still poorly defined and is only slowly emerging.