BACKGROUND:
Venom immunotherapy (VIT) provides widespread protection against systemic anaphylactic reactions after a sting of the respective insect. This effect is attributed to a shift from T(H)2 to T(H)1. However, because basophils also produce and release cytokines, such as IL-4 and IL-13, they may be part of the cytokine network. The cytokines may regulate basophilic granulocytes, as suggested by the presence of cytokine receptors IL-2Ralpha, GM-CSFRalpha, IL-1RII, IL-3R, IL-4R, IL-5R, and IL-6R on basophils from nonallergic donors.
OBJECTIVE:
The purpose of this study was to demonstrate that human basophils from subjects allergic to wasp venom undergoing VIT are regulated by cytokines, as shown by the alteration of the expression of cytokine receptors (and other markers).
METHODS:
The expression of the surface interleukin receptors and activation antigens on basophils from 19 nonallergic subjects and 48 patients with wasp venom allergy was investigated before, immediately after, and 1 week after VIT (20 patients only).
RESULTS:
Basophilic granulocytes in allergic subjects, compared with those in healthy persons, showed elevated expression of CD32 (FcgammaRII), CD122 (IL-2Rbeta), CD124 (IL-4Ralpha), CD130 (IL-6 and 11Rbeta), CD154 (CD40L), and HLA-DR. Activation of basophils clearly increased during VIT indicated by increased expression of CD32, CD33, CD35 (CR1), CD63, CD116 (GM-CSFRalpha), CD122, CD124, CD130, and CD154. HLA-DR expression also tended to increase. The expression of IL-5R (CD125) decreased. A significant decrease of the basophilic surface antigens CD11c, CD32, CD35, CD63, CD116, CD122, CD124, CD130, and CD132 (interleukin receptor gamma) was detected 1 week after the end of rush VIT.
CONCLUSION:
The rise in CD63 during VIT indicates a partial basophil degranulation with release of stored protein mediators, including IL-4. IL-4 may cause a transient upregulation of different surface antigens in an autocrine manner. Thereafter, cytokines released by T cells, which as a result of VIT have changed from a T(H)2 type to a more T(H)1 type, downregulate the activation of the basophilic granulocytes.