Soluble CD30 and CD23 in cord blood are not related to atopy in early childhood

Abstract

Atopic disease, including atopic dermatitis (AD), is associated with a T-helper 2 (Th2)-dependent immune response. The cytokine receptor CD30 appears to be preferentially expressed on, and its soluble form (sCD30) released by, Th2 cells. Therefore, sCD30 may be a potential marker for atopic disorders. The aim of this study was to test the hypothesis that the sCD30 level in cord blood could be used to predict the development of atopy or AD in early childhood. In a case-control study, levels of sCD30, as well as soluble low-affinity immunoglobulin E (IgE) receptor (sCD23), interleukin-4 (IL-4) and IgE, were measured in cord blood in 35 children who subsequently developed allergic sensitization and AD before the age of three, and the results were compared to those of 35 matched children without a history of atopy. There was no difference in cord blood levels of sCD30 between controls (32.5 U/ml; 19.7-80.1) and children with subsequent atopy and AD (32.2 U/ml; 22-75.9) (median; quartiles). The concentration of sCD30 showed no relation to the levels of total IgE, sCD23 or IL-4. Levels of sCD23 were similar in children with subsequent atopy (60.2 U/ml; 44.5-76.8) and controls (55.2 U/ml; 38.3-72.5), whereas IL-4 was detectable in 10 of the atopic children and in only two of the controls (p <0.05). In conclusion, cord blood levels of sCD30 or sCD23 do not seem to be related to the subsequent development of atopy or AD at the age of three.

Cord Blood Soluble CD14 Predicts Wheeze and Prolonged Cough in Young Children: The PATCH Study

“…However, because of its low sensitivity, it is not a reliable predictive marker of atopic diseases [21][22][23] . Various soluble cytokines and cytokine receptors in cord blood, such as sCD30, sCD23 and the IL-4 receptor, have also been studied, but none has been found to be a significant predictive factor for atopic disorders [24,25] . However, the presence of sCD14 in early life may be related to further atopy [26] , although its predictive value for atopic disease and the corresponding optimal cut-off point require further research.…”

IL-4 and IL-13 Differentially Regulate TLR-Induced Eosinophil-Basophil Differentiation Of Cord Blood CD34+ Progenitor Cells

“…Our previous findings that atopicrisk infants produce fewer LPS-induced Eo/B CFU, and stimulation of non-atopic mononuclear cells with IL-4 inhibits LPS signalling, much like that found in the cells of the atopic counterparts [24] add credence to our use of IL-4 to recapitulate the maternal allergic microenvironment in utero [12,13]. Therefore, our present findings suggest IL-4, which can be found in the CB of at-risk infants who subsequently go on to develop disease [12,13] has an inhibitory effect on Eo/B CFU [28,29] through altered CB CD34…”

“…+ cells via autocrine activation of MAPK [11] and atopic at-risk infants have elevated T H 2 cytokines in their CB [12,13], we were interested in what effect these cytokines may have on LPS-induced Eo/B CFU [10]. Relatedly, maternal cytokines (which can be transferred to the CB) have been shown to play instructive roles in fetal immune development.…”

“…These cytokines are involved in IgE production [16] and eosinophil recruitment to the airways [17]. The expression of IL-4 is increased in the airways of allergic subjects [18] and in the CB of at-risk infants who subsequently develop atopic disease [12,13]. Although these cytokines have recently been shown to influence human CB CD34 + cell chemotaxis [19] and murine bone marrow (BM) Eo/B CFU formation ex vivo [20] it is unclear what effects IL-4 or IL-13 might have on LPS-induced Eo/B CFU formation from human CB CD34 + cells.…”

Expression of CD21 and CD23 during Human Fetal Development

“…In contrast to membrane CD23, sCD23 enhances IgE production (22,25). Soluble CD23 levels were not examined in this study, but, in a previous study, cord sCD23 levels were reduced compared with the adult (27). As the processing of mCD23 to sCD23 may have an IgEenhancing effect (25), restriction of this pathway on fetal/ neonatal B cells could contribute to reduced IgE production.…”