IgE+ B cells are scarce, but allergen-specific B cells with a memory phenotype circulate in patients with allergic rhinitis.

BACKGROUND: Despite the critical role of immunoglobulin E (IgE) in allergy, circulating IgE+ B cells are scarce. Here, we describe in patients with allergic rhinitis B cells with a memory phenotype responding to a prototypic aeroallergen. METHODS: Fifteen allergic rhinitis patients with grass pollen allergy and 13 control subjects were examined. Blood mononuclear cells stained with carboxyfluorescein diacetate succinimidyl ester (CFSE) were cultured with Bahia grass pollen. Proliferation and phenotype were assessed by multicolour flow cytometry. RESULTS: In blood of allergic rhinitis patients with high serum IgE to grass pollen, most IgE(hi) cells were CD123+ HLA-DR(-) basophils, with IgE for the major pollen allergen (Pas n 1). Both B and T cells from pollen-allergic donors showed higher proliferation to grass pollen than nonallergic donors (P = 0.002, and 0.010, respectively), whereas responses to vaccine antigens and mitogen did not differ between groups. Allergen-driven B cells that divided rapidly (CD19(mid) CD3(-) CFSE(lo) ) showed higher CD27 (P = 0.008) and lower CD19 (P = 0.004) and CD20 (P = 0.004) expression than B cells that were slow to respond to allergen (CD19(hi) CD3(-) CFSE(mid) ). Moreover, rapidly dividing allergen-driven B cells (CD19(mid) CFSE(lo) CD27(hi) ) showed higher expression of the plasmablast marker CD38 compared with B cells (CD19(hi) CFSE(mid) CD27(lo) ) that were slow to divide. CONCLUSION: Patients with pollen allergy but not control donors have a population of circulating allergen-specific B cells with the phenotype and functional properties of adaptive memory B-cell responses. These cells could provide precursors for allergen-specific IgE production upon allergen re-exposure.

Providing supplemental milk to piglets preweaning improves the growth but not survival of gilt progeny compared with sow progeny.

Gilt progeny have lighter weaning weights and greater postweaning medication and mortality rates compared with the progeny of older parity sows. Because weaning weight has been positively correlated with postweaning survival, this study aimed to determine whether the provision of supplemental milk preweaning could improve weaning weight and subsequent weights as well as postweaning survival of gilt progeny. The study was replicated in summer and winter as the effects of supplemental milk were expected to vary with season. The progeny of 80 gilts (parity 0) and 80 sows (parity 2 to 5) were allocated to both treatments: with or without supplemental milk in these 2 seasons with 5 sheds/season. Litter size was standardized (10 to 11 piglets) and each piglet was weighed at birth, d 21, weaning (4 wk), and 10 wk of age. Medications and mortalities were recorded both preweaning and postweaning. Pigs were housed within treatment groups postweaning, and ADFI and G:F were measured. Gilt progeny were 200 g lighter at birth in both replicates (P < 0.001) and were 500 g lighter at weaning in the winter replicate (P < 0.05) compared with sow progeny. The provision of supplemental milk improved weaning weight for both gilt and sow progeny by 800 g in summer (P < 0.05) and by 350 g in winter (P < 0.05). This improvement in weaning weight had no effect on the incidence of death or disease in milk-supplemented progeny of either gilts or sows (P > 0.05). Supplemental milk disappearance (the daily difference between the volume of milk provided and the residue left in the drinker) was greater in summer than winter (by 130 mL/piglet d(-1); P < 0.05) as were the associated weaning weight benefits. The weaning weights of supplemented gilt progeny reached or exceeded that of nonsupplemented sow progeny. Gilt progeny had greater postweaning mortality (2.6%) and medication rates (6.2%) than sow progeny (1 and 2.2%, respectively; both P < 0.05) in both seasons, but medication rates were greater in winter (7.2%) for both treatment groups than in summer (1.9%; P < 0.05). Gilt progeny also had less postweaning ADFI than sow progeny in winter (528 and 636 g, respectively; P < 0.05) with no dam parity effect on G:F (both P > 0.05). The hypothesis that supplemental milk provision did increase gilt progeny weaning weight was supported (especially in summer) but the supplementation had no effect on postweaning weights and survival. Efforts to improve gilt progeny postweaning growth and survival need to be aimed at improving health and immunity, not just weaning weight.

Oral immunization with xenogeneic antibodies stimulates the production of systemic and mucosal anti-idiotypic antibodies.

The humoral and mucosal immune responses to oral immunization with xenogeneic antibodies were studied using an animal model in which female rabbits were fed daily doses of the MOPC-315 murine IgA antibody, and were mated during the course of the feeding programme. Serum and colostrum samples were assayed for the presence of anti-idiotypic antibodies by ELISA assay, before and after depletion of anti-IgA antibodies, by affinity chromatography using another murine IgA idiotype. It was shown that all animals responded to exposure to the MOPC-315 idiotype with the production of serum anti-murine immunoglobulin antibodies and that four of six animals produced serum anti-idiotypic antibodies. That the immune response included antibodies directed against the antigen-binding site was confirmed by competition ELISA assay. Mucosal IgG and IgA anti-immunoglobulin antibodies were present in milk from all antibody-fed rabbits tested, and IgA anti-idiotypic antibodies were detectable in the colostrum of one rabbit. The results provide some support for the hypothesis that human exposure to xenogeneic antibodies, most commonly bovine milk immunoglobulins, may provoke the production of anti-idiotypic antibodies, and that such exposure may lead to disturbances of immune regulation.

Bovine milk, including pasteurised milk, contains antibodies directed against allergens of clinical importance to man.

Pasteurised and raw bovine milk and bovine colostrum samples were assayed by enzyme-linked immunoassay for the presence of antibodies directed against a selection of allergens of importance in human atopic disease. Samples were tested for the presence of antibodies directed against or cross-reacting with ryegrass pollen, house dust mites, Aspergillus mould and wheat proteins. Antibodies of each specificity were detected in every sample tested, including all samples of commercial pasteurised milk. The results are discussed with reference to a hypothesis that dietary xenogeneic antibodies may play a role in the emergence of some human atopic disease, and the recent demonstration that oral immunisation with xenogeneic antibodies may lead to the production of anti-immunoglobulin antibodies including anti-idiotypic antibodies.