Data from: Flexibility of fetal tolerance: Immune function during pregnancy varies between ecologically distinct populations

Background and objectives: Among placental mammals, females
undergo immunological shifts during pregnancy to accommodate the fetus
(i.e. fetal tolerance). Fetal tolerance has primarily been characterized
within post-industrial populations experiencing evolutionarily novel
conditions (e.g. reduced pathogen exposure), which may shape maternal
response to fetal antigens. This study investigates how ecological
conditions affect maternal immune status during pregnancy by comparing the
direction and magnitude of immunological changes associated with each
trimester among the Tsimane (a subsistence population subjected to high
pathogen load) and women in the United States. 
Methodology: Data from the Tsimane Health and Life History
Project (N=935) and the National Health and Nutrition Examination
Survey (N=1395) were used to estimate population-specific effects of
trimester on differential leukocyte count and C-reactive protein (CRP), a
marker of systemic inflammation.  Results: In both
populations, pregnancy was associated with increased neutrophil
prevalence, reduced lymphocyte and eosinophil count, and elevated CRP.
Compared to their US counterparts, pregnant Tsimane women exhibited
elevated lymphocyte and eosinophil counts, fewer neutrophils and
monocytes, and lower CRP. Total leukocyte count remained high and
unchanged among pregnant Tsimane women while pregnant US women exhibited
substantially elevated counts, resulting in overlapping leukocyte
prevalence among all third-trimester individuals.  Conclusions
and implications: Our findings indicate that ecological
conditions shape non-pregnant immune baselines and the
magnitude of immunological shifts during pregnancy via developmental
constraints and current trade-offs. Future research should investigate how
such flexibility impacts maternal health and disease susceptibility,
particularly the degree to which chronic pathogen exposure might dampen
inflammatory response to fetal antigens.