Peanut allergy

In population-based studies from the USA, self-reported peanut allergy in children rose from 0.4% in 1997 to 0.8% in 2002 [21]. In the UK, prevalence rates for peanut allergy are in excess of 1%. Data from England points in the same direction with a twofold increase in reported peanut allergy. 

Sicherer SH, Sampson HA Peanut allergy emerging concepts and approaches for an apparent epidemic. J Allergy Clin Immunol 2007 120 491-505. Liew WK, Williamson E. Tang ML Anaphylaxis fatalities and admissions in Australia. J Allergy Clin Immunol 2009 123 434-442. 

Does skin prick test reactivity to purified allergens 64 correlate with clinical severity of peanut allergy ... 

Hourihane, J. O B., Recent advances in peanut allergy. Curr. Opinion Allergy Clin. Immunol., 2, 227, 2002. 

Allergies to soy may be a concern for some patients, and there may be a cross-reaction with peanut allergy. Bloating and gas occur, especially in those unaccustomed to soy products. 

There is some tolerance in the immune system, otherwise it could react unnecessarily to any foreign, large molecule such as those in food or the air (there are people who do indeed show hypersensitivity reactions to such things, hence hay fever, gluten intolerance, and peanut allergy). If only the antigen is present, the T cell may well ignore it. 

Howell, W. M., Turnen, S. J., Hourihane, J. O., and Warner, J. O. 1998. HLA classes DRB1., DQB1 and DPB Genotypic associations with peanut allergy (evidence for family-based and case control study). Clin Exp Allergy 28 156-162. 

Therefore this peanut-allergy model in C3H/HeJ mice was further used in many studies that focused on more mechanistic-, prophylactic-, or therapeutic aspects. In studies of van Wijk et al. (2004), it was observed that both Thl and Th2 phenomena were involved in the development of peanut allergy in the C3H/HeJ mice model. In a subsequent study in this peanut allergy C3H/HeJ mice model, it was shown by van Wijk et al. (2005) that the co-stimulatory molecule CTLA-4, predominantly expressed on activated T cells, is not the crucial factor in preventing sensitization to food allergens, but rather plays a pivotal role in regulating the intensity of a food allergic sensitization response. 

Helm, R.M., Furuta, J.S., Ye, J. et al. 2002. A neonatal swine model for peanut allergy. J Allergy Clin Immunol 109 136-142. 

Li, X.M., Srivastava, K., Grishin, A. et al. 2003a. Persistant protective effect of heat-killed Escherichia coli producing engineered , recombinant peanut proteins in a murine model of peanut allergy. J Allergy Clin Immunol 112 159-167. 

B. Proust, D. A. Moneret-Vautrin, A. W. Burks, B. Bihain, H. A. Sampson, and G. Kanny. 2006. Predictive value of skin prick tests using recombinant allergens for diagnosis of peanut allergy. J Allergy Clin Immunol 118 (l) 250-256. 

Roy, K., H. Q. Mao, S. K. Huang, and K. W. Leong. 1999. Oral gene delivery with chitosan— DNA nanoparticles generates immunologic protection in a murine model of peanut allergy. Nat Med 5 (4) 387-391. 

Skolnick, H.S., Conover-Walker, M.K. Koerner, C.B., Sampson, H.A., Burks, A.W., and Wood, R.A. 2001. The natural history of peanut allergy. J Allergy Clin Immunol 107 367-374. 

Burks, A.W. 2003. Peanut allergy A growing phenomenon. J Clin Invest 111 950-952. 

Emmett, S.E., Angus, F.J., Fry, J.S., and Lee, P.N. 1999. Perceived prevalence of peanut allergy in Great Britain and its association with other atopic conditions and with peanut allergy in other household members. Allergy 54 380-385. 

Hourihane, J.B., Aiken. R., Briggs, R. et al. 2007. The impact government advice to pregnant mothers regarding peanut avoidance on the prevalence of peanut allergy in United Kingdom children at school entry. J Allergy Clin Immunol 119 1197-1202. 

Peeters, K.A.B.M., Kunlst, A.C., Rynja, F.L., Bruijnzeel-Koomen, C.A.F.M., and Koppelman, S.J. 2004. Peanut allergy Sensitization by peanut oil-containing local therapeutics seems unlikely. J Allergy Clin Immunol 113 1000-1001. 

Wensing, M., Knulst, A.C., Piersma, S., O Kane, R, Knol, E.R, and Koppelman, S.J. 2003. Patients with anaphylaxis to pea can have peanut allergy caused by cross-reactive IgE to vicilin (Ara hi). J Allergy Clin Immunol 111 420 -24. 

Yu, J.W., Kagan, R., Verreault, N. et al. 2006. Accidental ingestions in children with peanut allergy. J Allergy Clin Immunol 118 466 -72. 

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