Modulation of immune function by dietary lectins in rheumatoid arthritis.
Despite the almost universal clinical observation that inflammation of the gut is frequently associated with inflammation of the joints and vice versa, the nature of this relationship remains elusive. In the present review, we provide evidence for how the interaction of dietary lectins with enterocytes and lymphocytes may facilitate the translocation of both dietary and gut-derived pathogenic antigens to peripheral tissues, which in turn causes persistent peripheral antigenic stimulation. In genetically susceptible individuals, this antigenic stimulation may ultimately result in the expression of overt rheumatoid arthritis (RA) via molecular mimicry, a process whereby foreign peptides, similar in structure to endogenous peptides, may cause antibodies or T-lymphocytes to cross-react with both foreign and endogenous peptides and thereby break immunological tolerance. By eliminating dietary elements, particularly lectins, which adversely influence both enterocyte and lymphocyte structure and function, it is proposed that the peripheral antigenic stimulus (both pathogenic and dietary) will be reduced and thereby result in a diminution of disease symptoms in certain patients with RA.
Cordain
L
L
Department of Health and Exercise Science, Colorado State University, Fort Collins 80523, USA. cordain@cahs.colostate.edu
Toohey
L
L
Smith
M J
MJ
Hickey
M S
MS
D000941:Antigens / Q000276:immunology; D001172:Arthritis, Rheumatoid / Q000235:genetics / Q000276:immunology*; D004751:Enteritis / Q000276:immunology*; D020895:Enterocytes / Q000276:immunology; D020022:Genetic Predisposition to Disease; D006801:Humans; D007108:Immune Tolerance; D037102:Lectins / Q000276:immunology*; D008214:Lymphocytes / Q000276:immunology; D018716:Molecular Mimicry / Q000276:immunology
D000941:Antigens; D037102:Lectins