Biomedical Engineering Reference
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secondary pathogen infection. During a secondary infection, memory T lympho-
cytes in peripheral tissues (i.e., outside of draining lymphoid nodes) are activated
by pro-inflammatory cytokines (IL12, IL18, and type-1 interferons) produced by
innate immunocytes. Resident memory CD8
+
T cells can also be directly activated
by dendritic cells together with CD4
T cells recruited to the infection site.
Antigen-specific memory T cells then interact with antigen-bearing dendritic cells
to generate a local, secondary effector T-cell response to limit pathogen replication
prior to arrival of secondary effector T cells from lymph nodes [
235
]. Because these
tissular sentinels release cytokines and chemokines, peripheral memory T cells alert
immunocytes. They quickly recruit circulating memory T cells (antigen-specific or
not) before attracting effector T cells from draining lymph nodes to the inflammation
site.
The number of antigen-specific memory T cells decreases at peripheral sites
after pathogen removal. Antigen-specific memory T cells are relatively quiescent.
Nevertheless, they undergo changes in phenotype, function, and location. Memory
T-cell pool specific for a given antigen is maintained by interleukins IL7 and
IL15 [
235
].
+
Subpopulations of Memory T Lymphocytes
The antigen-specific memory T-cell pool can be decomposed into peripheral and
lymphoid tissue-resident populations that do not live in similar environments. In
lung alveoli, memory T cells are exposed to near atmospheric oxygen concentrations
and surfactant proteins, such as SPa1 and SPd.
116
Memory T lymphocytes of adaptive immunity ensure antigen-specific protection
and rapid recall response against repeated invasions of pathogens. Both viral
and bacterial infections stimulate Ifn
T lymphocytes that can
differentiate into long-lived memory T cells. The long-lived CD8
γ+
,CD4
+
,CD8
+
+
memory T-cell
population is larger than that of CD4
+
memory T lymphocytes. Both CD4
+
and
CD8
+
memory T-cell subsets with distinct functional potentials arise from Ifn
γ+
T-cell progenitors [
234
].
Memory T lymphocytes determined after infection can be divided into 2 groups
based on expression of the lymphoid homing receptors L-selectin and CCR7 [
235
]:
(1) central memory L-selectin
T cells (T
CM
) that preferentially localize
in lymphoid tissues and (2) effector memory L-selectin
+
, CCR7
+
T cells (T
EM
)that
preferentially reside in peripheral tissues. Antigen-specific memory T lymphocytes
gradually convert to central memory T cells that are less able to migrate into
−
, CCR7
−
116
A.k.a. SftPa1 and SftPd surfactant proteins. Antigen-dependent and -independent mechanisms
contribute to the maintenance of peripheral memory CD8
+
T lymphocytes in lung airways.
Circulating memory CD8
+
T cells can migrate to airways upon stimulation by antigen located in
lung-draining lymph nodes, whereas a small number of systemic memory CD8
+
T cells migrate
to airways even in the absence of specific antigen.
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