R. Siegmund et al., Surface membrane antigen alteration on blood basophils in patients with Hymenoptera venom allergy under immunotherapy, J ALLERG CL, 106(6), 2000, pp. 1190-1195
Background: Venom immunotherapy (VIT) pro,ides widespread protection agains
t systemic anaphylactic reactions after a sting of the respective insect. T
his effect is attributed to a shift from T(H)2 to T(H)1. However, because b
asophils also produce and release cytokines, such as IL-4 and IL-13, they m
ay he part of the cytokine network. The cytokines may regulate basophilic g
ranulocytes, as suggested by the presence of cytokine receptors IL-2R alpha
, GM-CSFR alpha, 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 basophil
s from subjects allergic to wasp venom undergoing VIT are regulated by cyto
kines, as shown by the alteration of the expression of cytokine receptors l
and other markers).
Methods: The expression of the surface interleukin receptors and activation
antigens on basophils from 19 nonallergic subjects and 48 patients with wa
sp venom allergy was investigated before, immediately after, and 1 week aft
er VIT (20 patients only).
Results: Basophilic granulocytes in allergic subjects, compared with those
in healthy. persons, showed elevated expression of CD32 (Fc gamma RII), CD1
22 (IL-2R beta), CD124 (IL-4R alpha), CD130 (IL-6 and 11R beta), CD154 (CD4
0L), and HLA-DR. Activation of basophils clearly increased during VIT indic
ated by increased expression of CD32, CD33, CD35 (CR1), CD63, CD116 (GM-CSF
R alpha), 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, (SD122,
CD124, CD130, and CD132 (interleukin receptor gamma) was detected 1 week af
ter the end of rush VIT.
Conclusion: The rise in CD63 during VIT indicates a partial basophil degran
ulation with release of stored protein mediators, including IL-4. IL-4 may
muse a transient upregulation of different surface antigens in an autocrine
manner. Thereafter, cytokines released by T cells, which as a result of VI
T have changed from a T(H)2 type to a more T(H)1 type, downregulate the act
ivation of the basophilic granulocytes.