Profound deficit of IL10 at birth in children who develop childhood acute lymphoblastic leukemia

Childhood acute lymphoblastic leukemia (ALL) may originate via abnormal immune responses to infectious agents. It is unknown whether prenatal immune development may differ in children who develop the disease. The current study examines the association between neonatal cytokine profiles, a proxy measure for a child's prenatal immune development, and childhood ALL.

Neonatal blood spots of 116 childhood ALL cases and 116 controls living in California were ascertained. Eleven cytokines associated with Th1, Th2, and Th17 lymphocytes were measured using a multiplex bead-based assay. Unconditional logistic regression was done to estimate the odds ratio (OR) by measuring the association between neonatal cytokines and ALL adjusted for age, sex, race/ethnicity, and household income.

Of the 11 cytokines measured, 5 [interleukin (IL)4, IL6, IL10, IL12, and IL13] were detectable. Except for IL12, the other 4 cytokines were all significantly lower among cases than controls. In a multivariable model including the 5 cytokines, only IL10 remained independently associated with childhood ALL with an OR = 0.04, 95% CI: 0.01 to 0.18, comparing the highest tertile to the lowest tertile.

A child's neonatal level of IL10, a key regulator for modulating the intensity and duration of immune responses, is associated with his/her subsequent risk of developing ALL.

The current analysis shows that children with ALL may have a dysregulated immune function present at birth.