title: Regulatory roles of IL-12, IL-4 and IFN-gamma on IgE synthesis in atopic patients.
abstract: OBJECTIVE
  To investigate the mechanism of cytokine regulation in atopy by analyzing the effects of three major cytokines, IL-4, IL-12 and IFN-gamma on in vitro IgE synthesis of human peripheral blood mononuclear cell (PBMC) from normal individuals and atopic patients.
  
  
  METHODS
  We investigated 5 normal individuals and 22 atopic patients including 12 allergic asthma, 8 allergic rhinitis and 2 atopic dermatitis. Human PBMCs were separated and incubated in 96-wells culture plates with different cytokines. Cultured for 7 days, the supernatant was collected and the contents of IgE synthesized in vitro were detected.
  
  
  RESULTS
  There was no IgE synthesis in vitro of PBMC from all the normal individuals and 7 patients, however, other 15 patients' PBMC could produce IgE in vitro. We found that rhIL-4 could induce in vitro IgE synthesis of PBMC from all the normal individuals and 22 patients. rhIL-12 could inhibit IgE synthesis induced by rhIL-4. Further investigation of cytokine effects on IgE synthesis was conducted in 15 patients whose PBMCs did produce IgE in vitro (average level was 714 +/- 1105 ng/L). The following effects were observed: (1) 10 micrograms/L rhIL-4 could augment in vitro IgE synthesis from 714 +/- 1105 ng/L to higher level of 1483 +/- 1396 ng/L; (2) 20 micrograms/L rhIL-12 could inhibit in vitro IgE synthesis from 714 +/- 1105 ng/L to lower level of 452 +/- 969 ng/L; (3) rhIL-12 could block IgE synthesis induced by rhIL-4 to the level of 583 +/- 1084 ng/L; (4) 50 micrograms/L IFN-gamma could inhibit in vitro IgE synthesis from 714 +/- 1105 ng/L to the level of 461 +/- 1063 ng/L.
  
  
  CONCLUSIONS
  rhIL-4 could induce in vitro IgE synthesis, rhIFN-gamma could inhibit the in vitro IgE synthesis and rhIL-12 could antagonize rhIL-4 effect on in vitro IgE synthesis of PBMC from atopic patients.
authors.affiliation: Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing 100005, China.
authors.forename: M
authors.initials: M
authors.lastname: Liu
authors.forename: S
authors.initials: S
authors.lastname: Zheng
authors.forename: X
authors.initials: X
authors.lastname: Wang
authors.forename: Z
authors.initials: Z
authors.lastname: Wen
mesh_terms: D000328:Adult; D001249:Asthma / Q000378:metabolism*; D003876:Dermatitis, Atopic / Q000378:metabolism; D005260:Female; D006801:Humans; D007073:Immunoglobulin E / Q000096:biosynthesis*; D007371:Interferon-gamma / Q000494:pharmacology; D018664:Interleukin-12 / Q000494:pharmacology*; D015847:Interleukin-4 / Q000494:pharmacology*; D008297:Male; D011994:Recombinant Proteins / Q000494:pharmacology; D012221:Rhinitis, Allergic, Perennial / Q000378:metabolism
chemical_list: D011994:Recombinant Proteins; D018664:Interleukin-12; D015847:Interleukin-4; D007073:Immunoglobulin E; D007371:Interferon-gamma