Serum levels of the soluble low affinity receptor for IgE and soluble interleukin‐2 receptor in childhood, and their relation to age, gender, atopy and allergic disease

Abstract

Identifying immune factors associated with the development of atopy can enhance our understanding of the in vivo mechanisms involved and may have utility in paradigms designed to prevent disease. Two candidates suggested for such roles are the soluble low affinity receptor for IgE (sCD23) and the soluble interleukin-2 receptor (sCD25). To assess serum levels of these factors blood samples were collected at birth and at age 6 in a large nonselected population from Tucson, AZ. Log mean sCD23 and sCD25 levels decreased from birth to age 6, (for sCD23 0.60 ffi 0.26pg/l, n = 340 and 0.53 + 0.28pg/l, n = 333 and for sCD25 1.95 i 0.14pM, n = 304 and 1.86 ffi 0.20pM, n = 327, for the two ages respectively. Anglo children had lower sCD23 levels at birth compared to Hispanic children (p < 0.01); no effect of gender was observed. Skin test reactivity at age 6 was directly related to sCD25 levels at age 6 (p = 0.007) and even levels at birth showed a similar trend (p = 0.06). These relations were distinct from any relation to total serum IgE. No relation was observed with sCD23 levels for either skin test reactivity or serum IgE. The prevalences of asthma, rhinitis and eczema by age 6 were unrelated to sCD25 or sCD23 levels. The results indicate that soluble CD23 and CD25 have higher levels at birth than later in childhood and that the development of skin test reactivity may be associated with regulatory mechanisms involving sCD25, whereas sCD23 was not similarly implicated.

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

“…The low‐affinity IgE receptor, CD23, is present on B cells and up‐regulated when B cells commit to IgE synthesis (23). The up‐regulation is accompanied with release of sCD23, which has been suggested as a marker of atopic disease (14,16). Consistent with other and larger studies, we were not able to demonstrate a relationship between levels of sCD23 in cord blood and later development of atopy (15,16).…”

“…The role of immunoglobulin E (IgE) as a predictor of atopic disease in early childhood is well established (13), and correlation between IgE and soluble low‐affinity IgE receptor (sCD23) has been demonstrated in individuals with allergic disease (14). However, only a few studies have evaluated whether sCD23 in cord blood may predict subsequent allergic sensitization and AD (15,16).…”

In search for predictive factors for atopy in human cord blood

“…Furthermore, Th2 related soluble cytokine and immunoglobulin receptors like soluble (s‐) CD30, sCD23 and sIL‐4 receptor (sIL‐4R) have been connected to atopic diseases in adults (26). These receptors have also been investigated in CB as putative predictors of atopy, but neither sCD30, sCD23 nor sIL‐4R CB levels were sufficient in predicting the onset of atopic diseases during infancy/early childhood (27–29). Some chemokines favouring the outcome or being involved in the maintenance of a Th2 immune response like thymus and activation‐regulated chemokine (TARC/CCL17), macrophage‐derived chemokine (MDC/CCL22), eotaxin (EOX/CCL11), monocyte chemotactic protein 1 (MCP‐1/CCL2), and interferon‐gamma‐(IFN‐ γ ) inducible protein 10 (IP‐10/CXCL10) are known to be elevated in adult atopic individuals especially at the exacerbation state of AD (3).…”

Increased serum IL‐10/IL‐12 ratio in wheezing infants

“…Several studies have found increased levels of sIL‐2R in serum and BAL‐fluid in children and adults with atopic eczema and asthma (10, 37), although other studies could not confirm this (38, 39). We were also unable to show an association between sIL‐2R and wheezing and skin rash in the first or second year of life.…”