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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.1103592


Received for publication November 25, 2003.

Accepted for publication February 16, 2004.


Article

Aging and innate immune cells

Timothy P. Plackett *{dagger}{ddagger}, Eric D. Boehmer *, Douglas E. Faunce {dagger}{sect}, and Elizabeth J. Kovacs *{dagger}{sect}@

Departments of *Cell Biology, Neurobiology, and Anatomy and Surgery, {sect}Immunology and Aging Program, {dagger}Burn and Shock Trauma Institute, Loyola University Chicago, Maywood, Illinois; and {ddagger}Chicago College of Osteopathic Medicine, Midwestern University, Downers’ Grove, Illinois

@ To whom correspondence should be addressed. E-mail: ekovacs{at}lumc.edu.


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Abstract

The innate immune system serves an important role in preventing microbial invasion. However, it experiences significant changes with advancing age. Among the age-associated changes are: Aged macrophages and neutrophils have impaired respiratory burst and reactive nitrogen intermediates as a result of altered intercellular signaling, rendering them less able to destroy bacteria. Aged neutrophils are also less able to respond to rescue from apoptosis. Aged dendritic cells (DC) are less able to stimulate T and B cells. The altered T cell stimulation is a result of changes in human leukocyte antigen expression and cytokine production, and lower B cell stimulation is a result of changes in DC immune complex binding. Natural killer (NK) cells from the elderly are less capable of destroying tumor cells. NK T cells increase in number and have greater interleukin-4 production with age. Levels of various complement components are also altered with advancing age.

Key Words: immunosenescence • macrophage • dendritic cell • polymorphonuclear neutrophil




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