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Ann. N.Y. Acad. Sci., Annals PrePrint, published online ahead of print April 27, 2007 doi: 10.1196/annals.1409.014 Copyright © 2007 by the New York Academy of Sciences description
1 29 Lincoln Drive, Room 530, Bethesda, Maryland, 20892, United States 2 Laboratory of Mycobacterial Diseases and Cellular Immunology, CBER / U.S. FDA, Bethesda, Maryland, United States 3 Laboratory of Intracellular Parasites, NIAID / NIH, Hamilton, Montana, United States
* To whom correspondence should be addressed. E-mail: karen.elkins{at}fda.hhs.gov. PrePrint Abstract
Studies of immune responses to Francisella have been conducted for well over 50 years. Here, the parameters of innate and adaptive immune responses to Francisella are reviewed, emphasizing those that contribute directly to protection against infection. Although older literature provides a wealth of information on human immune responses to infection and vaccination, most recent information has been derived largely from studies in animals and using animal cells, particularly mice. In experimental animals, activation of macrophages, a major and probably preferred host cell for Francisella, appears central to control of infection. Thus, in animal models and in vitro studies using mouse macrophages, cytokines such as IFN- Key Words:
Francisella, T lymphocyte, B lymphocyte, protective immunity, macrophage, dendritic cell, natural killer cell, cytokine, chemokine
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and TNF-
, derived first from both non-specific cells such as natural killer cells and later from Francisella-specific T cells, collaborate to effect intracellular killing. In mice, intracellular killing mechanisms include reactive nitrogen and oxygen species, but killing mechanisms remain to be identified in humans. Ultimately both CD4+ and CD8+ T cells develop into Francisella-specific memory cells and are important for control of primary Francisella infection or vaccination-induced protection. The effector mechanisms invoked by either CD4+ and CD8+ T cells, beyond production of IFN-
