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Cytokines and the lung

Division of Pulmonary and Critical Care Medicine, University of Michigan Hospital, Ann Arbor, MI, USA

CORRESPONDENCE: G.B. Toews, Division of Pulmonary and Critical Care Medicine, University of Michigan Hospital, Ann Arbor, MI, USA. Fax: 1 7347644556

Received: July 31, 2001
Accepted August 1, 2001

Cytokines are signal molecules that induce movement, differentiation, growth and death of many cell types. Cytokines generate these effects through interactions with receptors, which relay a signal into the cell triggering a response.

Cytokine-receptor interactions are promiscuous; a combining site of any receptor can bind many ligands. Promiscuity allows for the generation of agonists, alternative ligands that activate a receptor in a way similar to the normal ligands and antagonists, ligands that bind to a receptor, but neutralize the effects of an agonist. Cytokine-receptor interactions induce many diverse (pleiotropic) effects. Cytokine-receptor interactions are redundant; several cytokines can perform the same function.

Mammalian hosts use cytokines to maintain homeostasis and to provide signals crucial to host responses to invading microbes and other injurious agents. Cytokines are the molecular messages, which: 1) initiate and amplify inflammatory and immune responses by recruiting and activating cells; 2) regulate the activation and differentiation of T- and B-lymphocytes, whose functions are crucial to specific cell-mediated immunity; and 3) initiate and regulate local repair processes critical to the resolution of inflammatory responses.

Further studies of cytokines and their receptors should provide a framework for therapeutic interventions in patients with dysregulated inflammatory responses.