CYTOKINES IN THE ACQUIRED-IMMUNODEFICIENCY-SYNDROME AND OTHER INFECTIOUS-DISEASES

The pathogenesis of several infectious diseases is frequently related not only to their etiological agents of viral, bacterial, or parasitic nature, but also to the host immune response. Both inflammatory responses and specific immune responses to the invading microorganisms are controlled by complex networks of intercellular signalling molecules, namely cytokines. This rapidly growing family of mediators includes lymphokines, interleukins, and molecules such as tumor necrosis factors and interferons. Patterns of cytokine production from antigen- or allergen-specific T lymphocytic cell clones have been identified, firstly in animal models and subsequently in man, and are commonly referred to as T(H)0, T(H)1, and T(H)2 profiles. The predominance of one of these profiles strongly influences the type of immune response (humoral versus cellular) and, at least in some experimental models, whether the immune response is protective or harmful. This is most convincingly demonstrated in models of parasitic diseases, but has also been hypothesized to be involved in the pathogenesis of human immunodeficiency virus infection and the acquired immunodeficiency syndrome. Earlier studies on human immunodeficiency virus infection revealed that the replicative capacity of this retrovirus, like the herpes viruses, is strongly influenced by the cytokine milieu of infected cells. Transcriptional and post-transcriptional regulation of human immunodeficiency virus expression by human cytokines are examples of the complex interdigitation of viruses with the host immune system.