Antigens elicit qualitatively distinct immune responses based on their portal ofentry (TABLE 1).Introduction of antigen systemically,whether by injection (subcutaneous or intramuscular) or injury,leads to local infiltration of inflammatory cells and specific immunoglobulin pro duction1 By contrast,antigens introduced at mucosal surfaces (such as the gastrointestinal and genitourinary tracts) elicit active inhibition ofthe immune response to those antigens,systemically.In 1946,Merill Chase2 showed that oral administration ofa CONTACT SENSITIZING AGENT (2,4-dinitrochlorobenzene) did not lead to sensi tization,but rather prevented the animal from eliciting an immune response to subsequent intracutaneous injections and cutaneous challenges (FIG.1).The specific induction ofthese regulated responses by administra tion ofantigen through the gastrointestinal tract is known as ORAL TOLERANCE.In the decades since the landmark experiment by Chase2 ,researchers have gained important insights into the mechanisms oftolerance.We now know that toler ance is a normal feature ofthe immune system at mucosal surfaces.Tolerance can also be generated through nasal and airway4 administration ofantigen. Two related forms oftolerance have also been described. Direct injection ofantigen into the portal vein can lead to systemic non-responsiveness to that antigen (portal tolerance)5 as can inoculation ofthe anterior chamber of the eye,in a phenomenon known as anterior chamber associated immune deviation (ACAID)6.
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