In 1937 Cooke, Loveless and Stull (1) reported that normal individuals respond to pollen-inoculations by forming immune antibody.

This antibody can inhibit the urticarial response of sensitized skin to pollen by interfering with the pollen-reagin reaction. (In the absence of immune antibody, skin inoculated with reagin-bearing serum from a hay-fever patient promptly develops erythema and a wheal when pollen-antigen is introduced.) Subsequent studies (2) showed that the cutaneous response fails to occur in the presence of immune serum because pollen is bound and inactivated by the immune antibody. This antibody was found to differ from reagin not only in its greater avidity for pollen-antigen and in its ability to unite with antigen without irritating surrounding tissue, but also in its rapid disappearance from skin into which it had been injected and in its capacity to resist temperatures that inactivate reagin.

1

Presented at the Twenty-eighth Annual Meeting of the American Association of Immunologists at Chicago, Illinois, on April 17th, 1941.

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