Immunology Notes
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Immune Cells
Clone Selection
Cell Signaling
AntiViral Defense
Influenza Defense
Drug allergy
Systemic Lupus
Autoimmune Diabetes
Food Tolerance
Food Allergy

Allergy Resources

Immunology Notes

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Food Allergy
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Autoimmune Diseases  Systemic Lupus

Systemic Lupus Erythematosis (SLE) is an immune-mediated disease that serves as a model for hypersensitivity diseases. The peak incidence of SLE is in women between the ages of 20 and 40 and who present with a typical malar rash, lymphadenopathy, arthralgias, fever, fatigue and will often complain of recurrent flu-like illness. As the disease advances, increased evidence of target organ damage can be found with protein and red cells in the urine, raised ESR, pleurisy, pericarditis, hair loss, associated with the appearance of circulating auto-antibodies, especially antinuclear.

SLE features circulating immune complexes and fits the model of delayed pattern food allergy (Type 3 and IV hypersensitivity mechanisms). Patients with type 3 pattern food allergy have lupus-like symptoms and signs for years, but only a small subgroup crosses over or decompensates into the more severe illness, SLE. The butterfly rash is common and is associated with cervical node enlargement. Arthralgias are associated with generalized aching and stiffness and infrequently joint swelling occurs. The type 3 food allergy pattern appears to be a milder manifestation of SLE and may not progress over many years. These patients only occasionally have ANA titers above 1:40.

A number of prescription drugs and several industrial chemicals are known to trigger autoimmune disease. Hydralazine, isoniazid, penicillamine, practolol and other drugs can induce SLE. While they may act as incomplete antigens and contribute to immune complex formation, the toxic effects of certain drugs on the complement system may also interfere with immune complex clearing and induce SLE indirectly.

SLE can be considered a disease of immune complex handling - immune complexes containing non-cellular antigens are inappropriately deposited in tissues, which are then damaged by inflammatory responses. A general thesis would suggest that foods, drugs and chemicals in the environment that promote the formation of immune complexes or impair the clearing of complexes induce autoimmune disease. Hydralazine, marketed as an anti-hypertensive drug, also occurs naturally in tobacco, smoke, mushrooms and may enter the food supply through contamination with plastics, dyes, and herbicides. Individual susceptibility would be influenced by the ability to metabolize the toxic chemical. Slow acetylators, for example, are more prone to hydralazine-induced SLE.

Bardana et al reported on autoimmune reactions induced by dietary antigens. They recalled that Sr. Wm. Osler had first suggested that dietary proteins were important in the pathogenesis of Henoch-Schonlein purpura and arthritis. They reported on an investigation of alfalfa-induced illness in monkeys A non-nutrient amino acid, L-canavanine, found in alfalfa seeds and sprouts, was identified as a trigger of an SLE-like syndrome. The severity of illness produced by canavanine in monkeys is remarkable; a hemolytic anemia was a consistent effect. Cooking alfalfa-containing foods may remove the problem since canavanine is heat labile.

In SLE-prone mice, removing milk protein, casein, from a standard laboratory diet had a dramatic benefit - 8% of the casein-fed mice survived at 24 months; 100% of the casein-free group survived. When the milk protein, casein, is digested, protein fragments or peptides can be potent players in immune networks. A casein peptide, beta-casomorphin 4-9, stimulates immune activity, creating hypersensitivity.


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Immunology Notes is part of the Alpha Education series developed by Environmed Research. The books are copyright by Environmed Research and all rights to reproduction by any means are reserved. We encourage readers to quote and paraphrase topics from Immunology Notes published online and expect proper citations to accompany all derivative writings. The author is Stephen Gislason MD. The date of the most recent publication is 2015. The URL to the book description is

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