Specific human IgE response after immunization with birch pollen in scid mice transplanted with human peripheral blood mononuclear cells-A model for human allergy?

C.B-17 scid mice were transplanted ip with human peripheral blood mononuclear cells. Some transplanted mice were immunized ip with birch pollen. Levels of total and birch pollen-specific human IgE were measured in serum. Low levels of total human IgE were detected after 9 days. 20 days after transplantation 12 out of 12 mice transplanted with cells from a birch pollen allergic donor showed higher but variable levels of total human IgE, and a low level of birch pollen specific IgE was detected in one mouse that had not been immunized. Immunization with birch pollen did not influence the level of total human IgE. In a different experiment, mice transplanted with cells from a donor with a high level of total IgE, but without birch pollen allergy, developed high levels of total IgE 49 days after transplantation, whereas no birch pollen specific IgE was found (two immunized, two non-immunized mice). In contrast, two of four mice given cells from two donors with birch pollen allergy, but with lower levels of total IgE, produced birch pollen-specific IgE after immunization. Thus, measurable levels of total human IgE were spontaneously produced in most scid mice transplanted with human peripheral blood mononuclear cells. Detectable levels of birch pollen specific human IgE appeared to be produced in occasional non-immunized scid mice transplanted with cells from allergic donors. In mice given cells from some allergic donors, half the mice produced human birch pollen specific IgE after immunization.

Serum immunoglobulin G subclasses and serum immunoglobulin A in acute bronchiolitis in infants.

Serum IgG subclasses and Serum IgA were studied in 43 infants with acute bronchiolitis and 20 healthy infants. IgG subclasses were determined by a capture ELISA and IgA was quantified by turbidimetry. IgG1 concentrations were significantly lower in infants with bronchiolitis than in normal infants. The other IgG subclasses and IgA did not differ between the groups. The subgroups of infants with bronchiolitis who had previously suffered from otitis media or bronchitis, had significantly lower IgG2 than the other infants with bronchiolitis. The same was found for infants with bronchiolitis who had suffered from three or more lower respiratory tract infections. In infants who had suffered from upper or lower respiratory infections before the acute bronchiolitis, IgA was significantly higher than in infants without previous respiratory infections. Ten infants with bronchiolitis (23%) had IgG1 deficiency, that is values below the lower reference limit calculated in a population of healthy Norwegian infants. No healthy infants had any IgG1 deficiency. No infant with bronchiolitis had IgG2 or IgG3 deficiency. The low IgG1 values found in infants with acute bronchiolitis, may be one cause for infants to be more susceptible to RS virus infections.