Abstract
Maternal RhD alloimmunization is an inflammatory response against protein antigens in fetal red blood cells (RBC). However, not all women become alloimmunized when exposed to RhD+ fetal RBC. Thus, this study aimed to evaluate levels of inflammatory chemokines in RhD− pregnant women with erythrocyte alloimmunization. CXCL8, CXCL9, CCL5, and CXCL10 levels were determined from cell culture supernatants by flow cytometry in 46 (30 non-alloimmunized RhD− and 16 previously alloimmunized RhD−) pregnant women. CXCL8 levels were significantly higher (P < 0.004), and CXCL9 (P < 0.008) and CXCL10 (P < 0.003) levels were significantly lower in alloimmunized pregnant women. No significant difference in CCL5 levels was detected between the groups. Fetal RHD genotyping was performed in the alloimmunized RhD− group by real-time PCR. Anti-D alloantibody was detected in 10 mothers and anti-D and -C in six mothers. Twelve fetuses were RHD positive and four were RHD negative. Further studies of serum chemokines and placenta tissue could provide a better understanding of the cells involved in the pathogenesis of maternal erythrocyte alloimmunization.
Highlights
Chemokines are essential to stimulate chemotaxis of leukocytes and initiate inflammatory responses [1, 2]
CXCL9 and CXCL10 levels were significantly higher in nonalloimmunized women (RhD−/IAT−), whereas CXCL8 levels were significantly higher in alloimmunized (RhD−/IAT+) pregnant women
We present novel findings on the expression of the chemokines CXCL9 (MIG), CXCL10 (IP10), CXCL8 (IL-8), and CCL5 (RANTES) in cell culture supernatants in RhD-alloimmunized pregnant women
Summary
Chemokines are essential to stimulate chemotaxis of leukocytes and initiate inflammatory responses [1, 2]. Chemokines are potent mediators of embryogenesis and neoangiogenesis and important for the recruitment of macrophages and NK, dendritic, and T cells to maternal decidua [1, 2]. There is increasing evidence suggesting a relationship between maternal inflammatory status and disease pathogenesis in pregnancy [3, 4]. It remains unclear why some pregnant women do not become alloimmunized during pregnancy even when exposed to high amounts of RhD-positive fetal red blood cells (RBC). Analysis of inflammatory chemokines could provide a better understanding of the pathogenesis of maternal erythrocyte alloimmunization. Maternal RhD alloimmunization is an immune response against protein antigens in fetal RBC [5]. Studies in murine models of RBC alloimmunization showed increased RBC antibody
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