Effects of nongenetic factors on immune cell dynamics in early childhood: The Generation R Study

Abstract

Our study identifies specific dynamic patterns of leukocyte subset numbers, as well as nongenetic determinants that affect these patterns, thereby providing new insights into the shaping of the childhood immune system.

Age at cytomegalovirus, Epstein Barr virus and varicella zoster virus infection and risk of atopy: The Born in Bradford cohort, UK

“…In exploratory studies of the same cohort, an impact of female sex and CMV infection on immune cell dynamics in early childhood has been demonstrated. 44 The combined evidence indicates that the sex-specific associations we have observed may provide clues about the mechanisms involved in the development of atopy. There is evidence that CMV influences anti-inflammatory mediators (viral and host IL-10).…”

“…In the Generation R cohort (population‐based cohort from foetal life onwards, in Rotterdam, the Netherlands), no interaction of sex and CMV infection was observed in relation to immune phenotypes but the children were tested at age 6 years, so differences by age at infection could not be investigated. In exploratory studies of the same cohort, an impact of female sex and CMV infection on immune cell dynamics in early childhood has been demonstrated …”

Age-associated distribution of normal B-cell and plasma cell subsets in peripheral blood

“…Donors with any sign or suspicion of immunologic or hematologic diseases (including an abnormal infection rate or a known history of allergies) were excluded from the study. In addition, a questionnaire with environmental factors that could potentially affect development of the immune system, 25,29,30 was conducted in children less than 4 years of age (n 5 36), with no differences observed in the frequency of these factors among the age groups evaluated (see Table E1 in this article's Online Repository at www.jacionline.org). Also, the exact dates of different vaccinations received were collected in a subset of 72 children.…”

“…23,24 This early wave of recently produced B cells is followed by increased numbers of memory B cells (MBCs) that rapidly increase from 2 months of life, remain high until age 5 years, and gradually decrease thereafter to adult-like values. [23][24][25][26] During adulthood, the number of immature/transitional and naive B cells remains stable, whereas MBC and newly generated plasma cell (PC) counts gradually decrease in subjects older than 60 years. 27,28 Thus far, accurate and robust detection of low PC counts in PB (eg, in infants) appeared to be a challenge, 23,25,26 and information on IgH isotypes and subclasses within MBC and PC subsets remains limited, 27 Here we dissected the PB compartments of MBCs and PCs into 38 distinct subsets expressing different IgH isotypes and their subclasses and investigated their distribution in a large series of normal cord blood (CB) and PB from healthy European donors aged 0 to 90 years.…”

The influence of Epstein‐Barr virus and cytomegalovirus on childhood respiratory health: A population‐based prospective cohort study

“…10,11 Moreover, both viruses drive memory T cell expansions in young children. 12,13 Therefore, infections with these viruses could lead to a disbalance in immune responses, specifically T-helper cell-mediated responses, and subsequently an increased risk of asthma. [2][3][4] A prospective cohort study demonstrated that EBV coinfection enhances immune maturation driven by CVM.…”