Food allergens may also trigger the development of autoimmune diseases in addition to food allergic diseases

Food allergens have been known to cause food allergy to allergic individuals. However, no medical research has before reported that food allergens may also trigger the development of autoimmune diseases.

In a joint effort,  Ye Qian, PhD, professor of dermatology, and Timothy Moran, MD, PhD, assistant professor of pediatrics, found that walnut allergen, in addition to inducing allergic diseases to certain individuals, could also promote autoantibody development in an autoimmune skin disease called pemphigus vulgaris. The researchers are the first to report that the allergen could promote the autoantibody development and subsequent autoimmune disease. The finding has been published in The Journal of Allergy and Clinical Immunology, which is the most-cited journal in the field of allergy and clinical immunology. The article has also been selected to be highlighted in the “Latest Research” section of the American Academy of Allergy, Asthma and Immunology website. 

Two major outcomes of a dysfunctional immune system are allergy and autoimmunity. Growing evidence suggests there are some connections between the development of these two abnormalities. One crucial aspect in the understanding of autoantibody development in autoimmune diseases is identifying the source of antigens that trigger and/or drive the autoimmune responses in these diseases. This finding reveals the allergen linkage between allergic responses and autoimmune responses. The study may ultimately result in identifying food allergen triggers for autoimmune diseases and lead to a dietary elimination therapy for autoimmune diseases. This investigation represents a great example of successful complementary multidisciplinary collaboration in translational research.  

Their study has also developed a new tool - revertant or germline monoclonal antibodies - to identify the potential inciting environmental antigens (including food allergens) which activate the naïve B cell precursors for autoreactive or allergen-specific antibodies. This will promote future identification of environmental inciting antigens for a much wider spectrum of allergic and autoimmune diseases, which can significantly advance our understanding of the etiological mechanism by which environmental antigens may trigger the development of allergic and/or autoimmune diseases. Their finding also suggests a novel role for allergen-avoidance strategies in the management of autoimmune diseases.