PMID- 15972499
OWN - NLM
STAT- MEDLINE
DCOM- 20050714
LR  - 20220331
IS  - 0019-9567 (Print)
IS  - 1098-5522 (Electronic)
IS  - 0019-9567 (Linking)
VI  - 73
IP  - 7
DP  - 2005 Jul
TI  - Saturation of immunoglobulin E (IgE) binding sites by polyclonal IgE does not 
      explain the protective effect of helminth infections against atopy.
PG  - 4106-11
AB  - One hypothesis for the decreased rates of atopy observed among helminth-infected 
      individuals is that parasite-induced polyclonal immunoglobulin E (IgE) 
      out-competes allergen-specific IgE for FcepsilonRI binding on basophils and mast 
      cells. In experiments with fresh blood drawn from filaria-infected patients, we 
      found no association between ratios of polyclonal to Brugia malayi antigen 
      (BmAg)-specific IgE (range, 14:1 to 388:1) and basophil responses to BmAg as 
      measured by histamine release. Using serum samples from a filaria-infected 
      patient who also had dust mite (Dermatophagoides pteronyssinus)-specific IgE 
      antibodies from time points with various ratios of polyclonal to D. 
      pteronyssinus-specific IgE (16:1 to 86:1), we demonstrated that increased ratios 
      of polyclonal to D. pteronyssinus-specific IgE did not attenuate basophil 
      sensitization as measured by D. pteronyssinus-specific histamine release. 
      Suppression of histamine release was likely not observed in either of these sets 
      of experiments because polyclonal to antigen-specific IgE ratios were not 
      sufficiently high, as concurrent passive sensitization of basophil experiments 
      required ratios of polyclonal to antigen-specific IgE of greater than 500:1 to 
      suppress basophil histamine release. Further, the intensity of IgE staining in 
      basophil populations from 20 patients with active filaria infections correlated 
      strongly with total serum IgE levels (rho = 0.698; P = 0.0024) with no plateau in 
      intensity of IgE staining, even though some patients had total IgE levels of 
      greater than 10,000 ng/ml. Our data therefore suggest that in helminth infections 
      (and in filarial infections in particular), the ratios of polyclonal to 
      allergen-specific IgE rarely reach those levels necessary to inhibit 
      allergen-specific IgE-FcepsilonRI binding and to suppress allergen-induced 
      degranulation of mast cells and basophils.
FAU - Mitre, Edward
AU  - Mitre E
AD  - Helminth Immunology Section, Laboratory of Parasitic Diseases, National Institute 
      of Allergy and Infectious Diseases, 4 Center Lane, Room 4/126, National 
      Institutes of Health, Bethesda, Maryland 20892, USA. emitre@niaid.nih.gov
FAU - Norwood, Stephanie
AU  - Norwood S
FAU - Nutman, Thomas B
AU  - Nutman TB
LA  - eng
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Infect Immun
JT  - Infection and immunity
JID - 0246127
RN  - 0 (Receptors, IgE)
RN  - 37341-29-0 (Immunoglobulin E)
SB  - IM
MH  - Animals
MH  - Basophils/physiology
MH  - Binding Sites
MH  - Dermatophagoides pteronyssinus/immunology
MH  - Helminthiasis/*immunology
MH  - Histamine Release
MH  - Humans
MH  - Hypersensitivity/*prevention & control
MH  - Immunoglobulin E/blood/*metabolism
MH  - Receptors, IgE/analysis/*metabolism
PMC - PMC1168579
EDAT- 2005/06/24 09:00
MHDA- 2005/07/15 09:00
PMCR- 2005/07/01
CRDT- 2005/06/24 09:00
PHST- 2005/06/24 09:00 [pubmed]
PHST- 2005/07/15 09:00 [medline]
PHST- 2005/06/24 09:00 [entrez]
PHST- 2005/07/01 00:00 [pmc-release]
AID - 73/7/4106 [pii]
AID - 1821-04 [pii]
AID - 10.1128/IAI.73.7.4106-4111.2005 [doi]
PST - ppublish
SO  - Infect Immun. 2005 Jul;73(7):4106-11. doi: 10.1128/IAI.73.7.4106-4111.2005.