Send to

Choose Destination
See comment in PubMed Commons below
Blood Cells Mol Dis. 2009 Mar-Apr;42(2):108-12. doi: 10.1016/j.bcmd.2008.10.005. Epub 2008 Nov 20.

Developmental immunotoxicity (DIT), postnatal immune dysfunction and childhood leukemia.

Author information

  • 1Department of Microbiology and Immunology, College of Veterinary Medicine, C5-135 VMC North Tower Road, Cornell University, Ithaca, NY 14853, USA.


The developing immune system is a sensitive target for environmentally-induced disruption producing postnatal immune dysfunction. Unique immune maturational events occur during critical windows of prenatal/perinatal development and environmentally-induced disruption of one-time events can have serious health consequences. Additionally, the specialized immunological conditions necessary to bring a semi-allogeneic fetus to term place restrictions on both the maternal and offspring immune systems. These features combine not only to increase the risk of early-life immune insult (ELII), which includes xenobiotically-induced developmental immunotoxicity (DIT), but also to influence the nature of DIT-associated diseases for the child. Exposure to certain toxicants as well as maternal infections and other pregnancy stressors is known to induce postnatal immune dysfunction. Because dysfunctional immune responses to childhood infections have been proposed to play a role in childhood leukemia, DIT is a potential risk factor for this disease. This review details the range of disease susceptibilities impacted by DIT and discusses the importance of effective DIT safety testing for drugs and chemicals as a preventative measure.

[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Support Center