Abstract

CONTENT ALERTS Receive: RSS Feeds, eTOCs, free email alerts (when new articles cite this article), more» Information about commercial reprint orders: http://iai.asm.org/site/misc/reprints.xhtml To subscribe to to another ASM Journal go to: http://journals.asm.org/site/subscriptions/ INFECTION AND IMMUNITY, Mar. 1996, p. 683–690 0019-9567/96/$04.00 0 Copyright 1996, American Society for Microbiology Vol. 64, No. 3 MATTHEW J. FENTON1 AND MARY W. VERMEULEN2* The Pulmonary Center, Boston University School of Medicine, Boston, Massachusetts 02118,1 and Pulmonary and Critical Care Unit, Massachusetts General Hospital, Charlestown, Massachusetts 021292 INTRODUCTION Robert Koch identified Mycobacterium tuberculosis as the causative agent of tuberculosis (TB) in 1882 and was the first to realize that the efficacy of his early tuberculin therapies depended largely on the strength of the patient’s immune response. Recent understanding of the roles played by leukocytes and the cytokines they secrete has revealed much about the delicate underlying balance between the strategies used by M. tuberculosis to survive within a host and the concomitant efforts of the host to kill it. In this article, we review the current state of understanding of the roles played by mononuclear phagocytes in response to inhaled M. tuberculosis. Archeological evidence indicates that TB has afflicted humans for thousands of years