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2014 ; 162
(1 Pt B
): 290-7
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English Wikipedia
Immunosenescence in monocytes, macrophages, and dendritic cells: lessons learned
from the lung and heart
#MMPMID25251662
Linton PJ
; Thoman ML
Immunol Lett
2014[Nov]; 162
(1 Pt B
): 290-7
PMID25251662
show ga
In the absence of an immune challenge, healthy, aged individuals have a
significantly higher basal inflammatory state where circulating levels of
cytokines, including IL-6, TNF-? and IL-1?, are elevated [1]. This progressive
pro-inflammatory state, termed "inflamm-aging", affects the phenotype/function of
cells present in the aged as well as renders the older individuals more
susceptible to a poor prognosis after systemic insults. Although it is important
to understand the mechanisms that underlie the progression of disease, most
preclinical analyses of disease therapies are performed in young adult mice that
have an intact, functional immune system. Oftentimes, this is not necessarily
representative of the immune disposition in the aged, let alone diseased, aged.
Herein, two distinct responses that are not only commonly associated with aging
but that also have dendritic cells and/or monocytes and macrophages as key
players are discussed: pulmonary infection and myocardial infarction. Although
studies of pulmonary infection in the aged have progressed significantly, studies
of monocytes and macrophages in inflammation and cardiac injury following
ischemia in the aged have not been as forthcoming. Nonetheless, several elegant
studies have established the dynamic role of monocytes and macrophages post
infarction. These will be discussed in light of what is known with aging.
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