The clinical relevance of IgG food allergy testing through ELISA - Enzyme-Linked Immunosorbent Assay

Townsend Letter for Doctors and Patients, Jan, 2004 by Raymond M. Suen, Shalima Gordon

The Gut Immune System

It is well known that a significant portion of ingested proteins from food reach the gut-associated lymphoid tissues (GALT), in an immunologically intact form capable of stimulating immune responses in the susceptible individual. This susceptibility rests in the competency of the immunoregulatory mechanisms of the GALT that normally prevent the induction of a hypersensitive response to otherwise innocuous food challenges. It is undesirable to be intolerant to the foods we eat. Mobilization of the GALT against food antigens defines loss of oral tolerance to foods, and may provoke injurious local and systemic immune responses. The gut mucosal response, particularly that involving an antibody response, is highly dependent on T cell help. (18) T helper pattern induced clonal expansion may proceed through a cell-mediated (Th1) response, humoral (Th2) response, or immune tolerance (Th3). (19) It is important to note that T cells of the mucosal lymphoid tissue are heavily biased toward a Th2 response. This accounts for the predominance of the protective IgA isotype in mucosal effector tissues. However, the phenotypic polarization of immunoglobulin producing B cells favoring IgA is heavily influenced by the cytokine profile present in the mucosal milieu. Interleukin-4 (IL-4) for example, promotes isotype switching to both IgG1 subclass and IgE (20) whereas, the cytokine transforming growth factor beta (TGF-[beta]) favors B cell class switching from IgG and IgE to IgA, thereby suppressing any potential for a Th1 or Th2 inflammatory response to dietary antigen.

Ideally the intestinal immune system can discriminate proteins in the food stream as innocuous and not of any pathogenic importance. It can be said in this case that a state of tolerance is achieved with suppression of IgE and IgG responses, and enhancement of a local secretory IgA antibody response. Certainly, the integrity of the mucosal barrier with its immune constituents in competent interplay is prerequisite for oral tolerance induction, and susceptibility to breakdown of oral tolerance varies individually. Loss of mucosal barrier integrity and genetic polymorphisms in markers of innate immunity, including that of the Fc[gamma]R class of IgG receptors, no doubt play a key role in abrogation of oral tolerance to dietary challenge. The biological mechanisms of food allergies are diverse and remain to be explored. Loss of tolerance, as exemplified by elevated food-specific IgG class antibodies is a breakdown of the GALT to distinguish antigens of nonpathogenic importance, abrogating the metabolic usefulness of the foods we eat, and instigating the potential for inflammatory and autoimmune conditions.

Effective assessment of food allergies, especially through IgG testing should be as routine for the practitioner as ordering a CBC (Complete Blood Count). Identification of elevated food-specific IgG antibodies is a means to identify loss of tolerance to dietary proteins, and provides the practitioner with a tool to direct care in the appropriate manner. Once identified, treatment of food allergies includes dietary rotation of compatible foods and avoidance of allergenic ones, in addition to cogent measures to reestablish tolerance.