Lectins, Agglutinins, and Their Roles in Autoimmune Reactivities

2015
Aristo Vojdani, PhD, MSc, CLS

ABSTRACT

Lectins are carbohydrate-binding proteins present throughout nature that act as agglutinins. Approximately 30% of our food contains lectins, some of which may be resistant enough to digestion to enter the circulation.

Because of their binding properties, lectins can cause nutrient deficiencies, disrupt digestion, and cause severe intestinal damage when consumed in excess by an individual with dysfunctional enzymes. These effects are followed by disruption of intestinal barrier integrity, which is the gateway to various autoimmunities.

Shared amino acid motifs between dietary lectins, exogenous peptides, and various body tissues may lead to cross-reactivity, resulting in the production of antibodies against lectin and bacterial antigens, followed by autoimmunity.

The detection of immunoglobulin G (IgG) or immunoglobulin A (IgA) antibodies against specific lectins may serve as a guide for the elimination of these lectins from the diet. It is proposed that this process can reduce the peripheral antigenic stimulus and, thereby, result in a diminution of disease symptoms in some—but not all—patients with autoimmune disorders. (Altern Ther Health Med. 2015;21(suppl 1):46-51.)

CONCLUSIONS

The author has provided extensive evidence linking dietary substances to the development of autoimmunities. Dietary glycoproteins, and other elements, can influence intestinal structure and function to allow increased translocation of both pathogenic and dietary antigens to the periphery, causing persistent immunological stimulation. Because of shared amino acid motifs among exogenous peptides, HLA-derived peptides, and self-tissue, crossreactivity may occur, thereby breaking immunological tolerance and resulting in the production of antibodies against lectin and bacterial antigens, followed by autoimmunity.

In genetically susceptible individuals, antigenic stimulation by lectins and other food antigens may result in the expression of RA by direct binding to the joint tissue, molecular mimicry, or by affecting TH17 plasticity.

This process may cause the activation of autoreactive lymphocytes and antibody production against both the food antigens and the endogenous peptides, thereby causing a malfunction in the immunological tolerance against selfantigens.

Detection of IgG or IgA antibodies against specific lectins may serve as a guide to clinicians for the elimination of lectins from their patients’ diets. It is proposed that the elimination of certain dietary elements, including lectins, that adversely influence both enterocyte and lymphocyte structure and function can reduce the peripheral antigenic stimulus and, thereby, result in a diminution of disease symptoms in some, but not all, patients with autoimmune disorders.

Therefore, if individuals have an autoimmune condition, they owe it to themselves to explore the link between lectins and autoimmunity in their journeys toward health and recovery.