ImmunologyTier 2Medical Sciences concept

Immunological adaptations of pregnancy (Th2 shift, hormone changes)

Core concept

Pregnancy requires immune tolerance of a semi-allogeneic fetus without global immunosuppression (the mother remains able to fight infection)
Th2-skewed shift at the maternal-fetal interface - favours humoral immunity, dampens the Th1/cell-mediated responses that would attack fetal (paternal) antigens
Mediated by progesterone, oestrogen, placental hCG; regulatory T cells (Tregs) expand to maintain tolerance to paternal antigens

Key detail

Trophoblast lacks classical HLA-A/B (avoids NK/T cell recognition) but expresses HLA-G (inhibitory, promotes tolerance)
Th1-mediated autoimmune conditions (rheumatoid arthritis, multiple sclerosis) often improve in pregnancy (Th2 shift) and flare postpartum (Th1 rebound)
Th2/antibody-mediated conditions (SLE) can worsen in pregnancy - the shift favours humoral autoimmunity

Clinical relevance

RA patient planning pregnancy - counsel that symptoms often improve in pregnancy but expect a postpartum flare
SLE patient - pregnancy is higher risk and needs closer monitoring (flare, antiphospholipid syndrome, neonatal lupus if anti-Ro/La positive)
Increased susceptibility to certain intracellular pathogens in pregnancy (listeria, malaria, some viral hepatitis present more severely)

Correlations

Rheumatoid arthritis and pregnancy
SLE and pregnancy, including neonatal lupus
HLA and transplant immunology
Regulatory T cell biology

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