Table 1: Summary of innate immune responses and their proposed role in control of or susceptibility to congenital CMV infection.

Innate immunity and susceptibility/protection in congenital CMV infection
Immune effectorMaternal/placental/fetal compartmentProposed effect on CMV transmission/disease

NK cells-CD56brightMaternal (pregnancy)
Uterine NK cells
(i) Decreased cytolytic potential
(ii) Increased risk of CMV transmission?

NK cells-NKG2C+Fetal compartment(i) Expansion of this NK subset in congenital and perinatal CMV
(ii) Correlation with symptomatic CMV disease?

Phagocytic cellsPlacental compartment(i) Neutrophils: possible role in defense
(ii) Macrophage: potentiates spread to syncytiotrophoblasts?

Toll-like receptorsMaternal compartment
Placental compartment
(i) TLR2 polymorphism; signaling to CMV glycoproteins; risk of CMV disease in transplant patients; increased transmission risk?
(ii) TLR3 polymorphism; decreased signaling to CMV antigens
(iii) TLR7 polymorphism: decreased antibody response to glycoprotein B?

Cytokines Chemokines DefensinsNeonatal compartment
Maternal compartment
Placental compartment
Placental-fetal interface
(i) IL-8 IF- may correlate with increased transmission risk
(ii) Increased maternal CCL-10 correlates with transmission
(iii) Increased placental MCP-1 expression correlates with fetal demise
(iv) Physiological increase in uterine IL-10 in pregnancy: increased risk of reactivation/transmission?
(v) Beta-defensins 8 and 31 proposed to be upregulated in amniotic fluid of asymptomatically congenitally infected infants