In this issue

Our first seven articles all focus on the early life origins of allergic disease. As has been described on innumerable occasions, infants destined to develop allergic disease and particularly eczema in the first 2 years of life, have altered T-cell responses even at birth. The most common finding has been of reduced c-interferon-producing T cells. Indeed, this was first highlighted in the early 1990 (1). The extent to which there is upregulation of IL4 and other Th2 cytokines is somewhat more contentious. We have published articles suggesting upregulation of Th2 responses in infants destined to have allergy (2). However, others have suggested that the Th2 dominance only evolves in the post-natal period (3). Our current article suggests both downregulation of c-interferon production and a higher percentage of interleukin-4-producing T cells in the cord blood of infants who subsequently developed eczema. To what extent this is affected by the evolving maternal immune response during pregnancy requires further elaboration. A study from Perth in Australia where many of the early life origins studies of Th1/Th2 balance have originated identifies that allergic mothers have a very different pattern of cytokine generation from non-allergic mothers as they progress through pregnancy. The allergic women had a sustained Th2 response with interleukin-13 generation, whereas non-allergic mothers had a progressive downregulation of the production of this cytokine. How this might relate to the interesting observation that IL-13 production in newborn babies destined to become allergic is lower than those in who do not develop allergy, remains to be established (4). Maternal environment during pregnancy may also affect outcomes. A study from Japan has suggested that pregnant women resident near a main road have children with an increased risk of asthma and eczema. Most studies hitherto have focused on post-natal pollutant exposure in increasing the risks of asthma. Perhaps more attention should now focus on antenatal impacts. Certainly, we have published previously on the effects of pregnancy smoking on risks of eczema (5). Maternal diet during pregnancy certainly has been a major focus in recent years. This was reviewed by the International Paediatric Allergy and Asthma Consortium (iPAC) (6). We have an article from Finland suggesting rather paradoxically that maternal consumption of citrus fruits during pregnancy may increase the risk of allergic sensitization, whereas vitamin D intake may have a beneficial effect. This rather contradicts observations of higher fresh fruit intake at least postnatally reducing wheeze and allergy in school children as in the Menorca study (7). A study from Japan suggests a high maternal intake of meat may increase the risk of eczema in offspring, but unlike a number of other studies showed no effect of maternal intake of fish or omega-3 polyunsaturated fatty acids (PUFA). However, differences in omega-3 to omega-6 PUFA s in human breast milk do have an impact on outcomes (8). Other constituents of breast milk clearly also have an impact on outcome. Wendy Oddy and Francisco Rosalez have conducted a systematic review of breast milk transforming growth factor (TGF)-beta highlighting the protective effects of both the b1 and b2 subtypes against allergy-related outcomes in infancy and early childhood, although not all studies are consistent with this analysis (9). Finally, a Japanese study highlights that reverse causation can confound studies attempting to identify protective effects of breast feeding against allergic disease that may explain many published negative studies (10). Our next four articles focus more on post-natal events in relation to development of allergy. We have one article on the effects of probiotics on intestinal IgA production and the potential impact this might have in reducing the risk of allergic sensitization. Delaying introduction of allergenic weaning foods has been a prevailing recommendation throughout the world as a means to prevent allergy. However, recent publications would suggest that this was not a sensible strategy. Indeed, early exposure to solid foods may be associated with less allergy as reviewed recently in the journal (11). We have Pediatr Allergy Immunol 2010: 21: 3–4