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Published online before print February 13, 2004
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Oral Infection and Immunity Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, Maryland
1Correspondence: OIIB, NIDCR, NIH, Building 30, Rm. 320, 30 Convent Drive, MSC4352, Bethesda, MD 20892-4352. E-mail: smwahl{at}dir.nidcr.nih.gov
Innate and adaptive immunity function to eliminate foreign invaders and respond to injury while enabling coexistence with commensal microbes and tolerance against self and innocuous agents. Although most often effective in accomplishing these objectives, immunologic processes are not fail-safe and may underserve or be excessive in protecting the host. Checks and balances to maintain control of the immune system are in place and are becoming increasingly appreciated as targets for manipulating immunopathologic responses. One of the most recognized mediators of immune regulation is the cytokine transforming growth factor-ß (TGF-ß), a product of immune and nonimmune cells. Emerging data have unveiled a pivotal role for TGF-ß as a perpetrator of suppression by CD4+CD25+ regulatory T (Treg) cells and in apoptotic sequelae. Through its immunosuppressive prowess, TGF-ß effectively orchestrates resolution of inflammation and control of autoaggressive immune reactions by managing T cell anergy, defining unique populations of Treg cells, regulating T cell death, and influencing the host response to infections.
Key Words: immunoregulation • apoptosis • leishmania
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