INTRODUCTION

Inflammation is a paradoxical process. This protective mechanism, whose absence spells prolonged illness or death, is also the cause of an enormous amount of morbidity worldwide with many idiopathic chronic inflammatory states, including asthma, autoimmune diseases (rheumatoid arthritis, multiple sclerosis, etc.), psoriasis, and inflammatory bowel disease, still awaiting a cure. The signs of inflammation were defined by the Roman encyclopaedist, Celsus, almost two millennia ago, and the humoral and cellular factors that drive inflammation have been under scrutiny since the middle of the nineteenth century. However, it was not until the 1950s that clues emerged as to how the enormously complex inflammatory/immune response, with its multiple cells and mediators (discussed in other chapters in this volume), was integrated and controlled. In the United States, the study of endotoxin-induced pyrexia (reviewed by Dinarello, 1989) and in the United Kingdom, the study of viral “interference” (reviewed by Gresser, 1997), led to the discovery of polypeptides with potent effects on cell behaviour. These proteins, interleukin (IL)-1 and interferon (IFN)α, respectively, were the forerunners of the enormous lists of proteins now known as cytokines that we recognise as inducing, and suppressing, inflammation (see Horst Ibelgauft's website, COPE, for a crash course in cytokines and Table 10.1). Cytokines can now be defined on the basis of their structural biology, or subdivided according to their historical naming/function, as in Table 10.1.