Biomedical Engineering Reference
In-Depth Information
The CD8
þ
T-cells are also the predominant T-cells infiltrating the
alveolar wall in smokers with COPD (8,93), although CD4
þ
T-cells are
also increased (8,95). Majo, studying lungs from nonsmokers and smokers
obtained at surgery, found that, similar to the airways (88), the only measur-
able difference between smokers with and without COPD was a substantial
increase in the number of total CD3
þ
and CD8
þ
T-cells in the alveolar wall
of smokers with COPD (Fig. 5). Furthermore, the total number of T-cells,
both CD8
þ
and CD4
þ
, increased with the amount smoked in smokers with
COPD, but not in healthy smokers, suggesting that the CD4
þ
T-cell is also
involved in the inflammatory process in COPD. This is an expected finding,
as CD4
þ
T-cell help is required for the cross-priming of CD8
þ
cytotoxic T-
cell responses, for maintaining their memory and for ensuring their survival
(see later).
Majo et al. (8), reasoning that as cytolytic CD8
þ
T-cells were involved
apoptosis should be present, quantitated and found an increased number of
apoptotic cells in the lungs of smokers with COPD which correlated with the
numbers of CD8
þ
cytolitic T-cells in the alveolar wall. This and other
reports, showing an increased number of structural lung cells undergoing
apoptosis in emphysematous lungs (96-98), support the idea that CD8
þ
Figure 5
Inflammatory cells in the alveolar wall (cells
=
mm alveolar wall) in
nonsmokers (NS), smokers without emphysema (SNE), and smokers with emphy-
sema (SE). Immunostains were used to identify neutrophils (elastase) all CD3
þ
(total
total T-cells), CD4
þ
, CD8
þ
, and
gd
T-cells. The distribution of inflammatory cells
differs from nonsmokers only in smokers with emphysema (p
<
0.05 by ANOVA).
(From Ref. 8.)