IgE recognition of autoantigens might augment allergic inflammation in the absence of exogenous allergen exposure. Among allergy and autoimmunity, there is disproportionate representation of males before puberty and females after puberty, suggesting a role for sex hormones. Hormone allergy is an allergic reaction where the offending allergens are one's own hormones. It is an immune reaction to the hormones, which can interfere with the normal function of the hormones. It can occur perimenstrually in women along with the variation in menstrual cycle. The perimenstrual allergies are about the cyclic abundance of the hormone causing a cyclic expression of allergic symptoms. The inflammatory mechanisms of allergic reactions to hormone allergens, which are intrinsic to the body, are the same as the mechanisms of allergic reactions to external allergens. 1. Introduction Allergy is a hypersensitivity disease based on body’s immune recognition of external allergens when they are inhaled, ingested, or contacted. Exposure of allergic individuals to external allergens can lead to immediate type inflammation caused by degranulation of mast cells via IgE-allergen immune complexes and the release of inflammatory mediators, proteases, and proinflammatory cytokines. However, allergic inflammation is reported to occur and persist in the absence of exposure to exogenous allergens and might paradoxically resemble a Th1-mediated chronic inflammatory reaction. There is evidence supporting the view that autoimmune mechanisms might contribute to these processes. IgE recognition of autoantigens might augment allergic inflammation in the absence of exogenous allergen exposure. Moreover, autoantigens that activate Th1-immune responses could contribute to chronic inflammation in allergy, thus linking allergy to autoimmunity [1]. Among allergy and autoimmunity, there is disproportionate representation of males before puberty and females after puberty, suggesting a role for sex hormones. After puberty, female allergy sufferings report more severe symptoms and a greater number of emergency room and hospital admissions than males [2–4]. Further majority of people living with autoimmune disorders are women as well. In fact, autoimmune diseases are among the leading causes of morbidity in females. An estimated 75 percent of those living with autoimmune diseases are females [5–7]. This gender dimorphism in the immune function of females could be due to sex hormones. In addition to their effects on sexual differentiation and reproduction, sex hormones influence the immune system. This
References
[1]
R. Valenta, I. Mittermann, T. Werfel, H. Garn, and H. Renz, “Linking allergy to autoimmune disease,” Trends in Immunology, vol. 30, no. 3, pp. 109–116, 2009.
[2]
G. Balzano, S. Fuschillo, G. Melillo, and S. Bonini, “Asthma and sex hormones,” Allergy, vol. 56, no. 1, pp. 13–20, 2001.
[3]
J. R. Bonner, “The epidemiology and natural history of asthma,” Clinics in Chest Medicine, vol. 5, no. 4, pp. 557–565, 1984.
[4]
A. J. Martin, L. A. McLennan, L. I. Landau, and P. D. Phelan, “The natural history of childhood asthma to adult life,” British Medical Journal, vol. 280, no. 6229, pp. 1397–1400, 1980.
[5]
D. L. Jacobson, S. J. Gange, N. R. Rose, and N. M. H. Graham, “Epidemiology and estimated population burden of selected autoimmune diseases in the United States,” Clinical Immunology and Immunopathology, vol. 84, no. 3, pp. 223–243, 1997.
[6]
C. C. Whitacre, “Sex differences in autoimmune disease,” Nature Immunology, vol. 2, no. 9, pp. 777–780, 2001.
[7]
C. C. Whitacre, S. C. Reingold, and P. A. O'Looney, “A gender gap in autoimmunity,” Science, vol. 283, no. 5406, pp. 1277–1278, 1999.
[8]
D. Kalogeromitros, A. Katsarou, M. Armenaka, D. Rigopoulos, M. Zapanti, and I. Stratigos, “Influence of the menstrual cycle on skin-prick test reactions to histamine, morphine and allergen,” Clinical and Experimental Allergy, vol. 25, no. 5, pp. 461–466, 1995.
[9]
C. Kirmaz, H. Yuksel, N. Mete, P. Bayrak, and Y. B. Baytur, “Is the menstrual cycle affecting the skin prick test reactivity?” Asian Pacific Journal of Allergy and Immunology, vol. 22, no. 4, pp. 197–203, 2004.
[10]
A. Haeggstr？m, B. ？stberg, P. Stjerna, P. Graf, and H. Hallén, “Nasal mucosal swelling and reactivity during a menstrual cycle,” ORL Journal for Oto-Rhino-Laryngology and Its Related Specialties, vol. 62, no. 1, pp. 39–42, 2000.
[11]
C. L. Haggerty, R. B. Ness, S. Kelsey, and G. W. Waterer, “The impact of estrogen and progesterone on asthma,” Annals of Allergy, Asthma and Immunology, vol. 90, no. 3, pp. 284–291, 2003.
[12]
Y. Cai, J. Zhou, and D. C. Webb, “Estrogen stimulates Th2 cytokine production and regulates the compartmentalisation of eosinophils during allergen challenge in a mouse model of asthma,” International Archives of Allergy and Immunology, vol. 158, no. 3, pp. 252–260, 2012.
[13]
A. Bouman, M. J. Heineman, and M. M. Faas, “Sex hormones and the immune response in humans,” Human Reproduction Update, vol. 11, no. 4, pp. 411–423, 2005.
[14]
M. H. H. Ensom, “Gender-based differences and menstrual cycle-related changes in specific diseases: implications for pharmacotherapy,” Pharmacotherapy, vol. 20, no. 5, pp. 523–539, 2000.
[15]
R. L. Wilder, “Hormones, pregnancy, and autoimmune diseases,” Annals of the New York Academy of Sciences, vol. 840, pp. 45–50, 1998.
[16]
N. Sinaii, S. D. Cleary, M. L. Ballweg, L. K. Nieman, and P. Stratton, “High rates of autoimmune and endocrine disorders, fibromyalgia, chronic fatigue syndrome and atopic diseases among women with endometriosis: a survey analysis,” Human Reproduction, vol. 17, no. 10, pp. 2715–2724, 2002.
[17]
M. R. Becklake and F. Kauffmann, “Gender differences in airway behaviour over the human life span,” Thorax, vol. 54, no. 12, pp. 1119–1138, 1999.
[18]
C. Nelson-Piercy, “Asthma in pregnancy,” Thorax, vol. 56, no. 4, pp. 325–328, 2001.
[19]
R. J. Troisi, F. E. Speizer, W. C. Willett, D. Trichopoulos, and B. Rosner, “Menopause, postmenopausal estrogen preparations, and the risk of adult- onset asthma: a prospective cohort study,” American Journal of Respiratory and Critical Care Medicine, vol. 152, no. 4, pp. 1183–1188, 1995.
[20]
V. Polacek, M. Jira, M. Fara, J. Strejcek, and R. Konigova, “Immunoglobulin E (IgE) in patients with severe burns,” Burns, Including Thermal Injury, vol. 13, no. 6, pp. 458–461, 1987.
[21]
E. Gaetjens and L. P. Pertschuk, “Synthesis of fluorescein labelled steroid hormone-albumin conjugates for the fluorescent histochemical detection of hormone receptors,” Journal of Steroid Biochemistry, vol. 13, no. 8, pp. 1001–1003, 1980.
[22]
M. Chalubinski and M. L. Kowalski, “Endocrine disrupters—potential modulators of the immune system and allergic response,” Allergy, vol. 61, no. 11, pp. 1326–1335, 2006.
[23]
S. I. Narita, R. M. Goldblum, C. S. Watson et al., “Environmental estrogens induce mast cell degranulation and enhance IgE-mediated release of allergic mediators,” Environmental Health Perspectives, vol. 115, no. 1, pp. 48–52, 2007.
[24]
F. Maranghi, M. Rescia, C. Macrì et al., “Lindane may modulate the female reproductive development through the interaction with ER-β: an in vivo-in vitro approach,” Chemico-Biological Interactions, vol. 169, no. 1, pp. 1–14, 2007.
[25]
J. F. Regal, D. G. Fraser, C. E. Weeks, and N. A. Greenberg, “Dietary phytoestrogens have anti-inflammatory activity in a guinea pig model of asthma,” Proceedings of the Society for Experimental Biology and Medicine, vol. 223, no. 4, pp. 372–378, 2000.
[26]
The British Dietetic Association, “Paediatric group position statement on the use of soya protein for infants,” Journal of Family Health Care, vol. 13, no. 4, p. 93, 2003.
[27]
P. Kastner, A. Krust, B. Turcotte et al., “Two distinct estrogen-regulated promoters generate transcripts encoding the two functionally different human progesterone receptor forms A and B,” EMBO Journal, vol. 9, no. 5, pp. 1603–1614, 1990.
[28]
T. Noriko and R. B. Theodore, “Covalent modification of proteins by ligands of steroid hormone receptors (HLCO ceils/retiok acid),” The Proceedings of the National Academy of Sciences of the United States of America, vol. 89, pp. 10807–10811, 1992.
[29]
J. Fishman, M. P. Osborne, and N. T. Telang, “The role of estrogen in mammary carcinogenesis,” Annals of the New York Academy of Sciences, vol. 768, pp. 91–100, 1995.
[30]
J. A. Lavigne, K. J. Helzlsouer, H. Y. Huang et al., “An association between the allele coding for a low activity variant of catechol-O-methyltransferase and the risk for breast cancer,” Cancer Research, vol. 57, no. 24, pp. 5493–5497, 1997.
[31]
E. L. Cavalieri, D. E. Stack, P. D. Devanesan et al., “Molecular origin of cancer: catechol estrogen-3,4-quinones as endogenous tumor initiators,” Proceedings of the National Academy of Sciences of the United States of America, vol. 94, no. 20, pp. 10937–10942, 1997.
[32]
B. T. Zhu and A. H. Conney, “Functional role of estrogen metabolism in target cells: review and perspectives,” Carcinogenesis, vol. 19, no. 1, pp. 1–27, 1998.
[33]
V. Unfer, G. C. di Renzo, S. Gerli, and M. L. Casini, “The use of progesterone in clinical practice: evaluation of its efficacy in diverse indications using different routes of administration,” Current Drug Therapy, vol. 1, no. 2, pp. 211–219, 2006.
