In healthy pregnancies, the semi-allograft foetus
is protected from maternal immune responses
by physiological immune tolerance (Figure 1).
11
A trimester-dependent increase in regulatory T
(CD4+CD25 high+; Treg) cell number has a key
role in this process;
12
moreover, this increase is
associated with physiological growth of the foetus.
13
These cells inhibit the activation of effector T
lymphocytes and natural killer (NK) cells, as well
as the differentiation of antigen-presenting cells.
14
Diminished numbers of Tregs in pregnancy were
associated with immunological rejection of the
foetus, low foetal birth weight or preeclampsia.
15
Of
note, the inhibitory effect of proliferating Treg cells
on NK cells
16
contributes to increased susceptibility to
viral infections during pregnancy, as observed in
the H1N1 influenza pandemic in 2009.
17
Healthy
pregnancy is characterised by a subtle shift in
T lymphocyte balance towards T helper (Th)2
phenotype, as a predominance of the Th1 cytokines
causes spontaneous abortion.
18,19
The circulating
number of the proinflammatory Th17 cells was
shown to be unaffected by healthy pregnancy,
20
but increased in pregnancies with adverse
outcomes such as preterm labour
21
and recurrent
spontaneous abortion.
22
Alterations of immune
state during pregnancy may cause changes in the
course of autoimmune diseases, e.g. systemic lupus
erythematosus or rheumatoid arthritis.