LYMPHOCYTE-TRANSFORMATION TEST WITH HOUSE-DUST MITE (DERMATOPHAGOIDES-PTERONYSSINUS) IN NORMAL-CHILDREN, ASTHMATIC-CHILDREN AND ASTHMATIC-CHILDREN RECEIVING HYPOSENSITIZATION
Hp. Vanbever et al., LYMPHOCYTE-TRANSFORMATION TEST WITH HOUSE-DUST MITE (DERMATOPHAGOIDES-PTERONYSSINUS) IN NORMAL-CHILDREN, ASTHMATIC-CHILDREN AND ASTHMATIC-CHILDREN RECEIVING HYPOSENSITIZATION, Clinical and experimental allergy, 23(8), 1993, pp. 661-668
In the first part of this study the proliferative response of lymphocy
tes (lymphocyte transformation test) to house dust mite (HDM) stimulat
ion in cultures was studied in normal children (n = 16), asthmatic chi
ldren who never received hyposensitization (HS) (n = 50) and asthmatic
children receiving HS with HDM for at least 6 months (n = 20). The re
sults are expressed as disintegrations per minute (d.p.m.) and as stim
ulation index (SI = d.p.m. in the presence of the allergen/d.p.m. in t
he control culture). A positive SI (> 2) was found in 54% of the asthm
atic children who never received HS, in 30% of the asthmatics receivin
g HS and in none of the normal children. Furthermore, between asthmati
cs with and without HS, the SI was not statistically different, althou
gh asthmatics without HS tended to have a higher SI (median value: 2.1
3 vs 1-38) (P= 0.10). In a second series of experiments the effect of
adding interleukin-2 (IL-2) to the lymphocyte cell culture was studied
in asthmatic children with and without HS. Interleukin-2 induced an a
dditional stimulatory effect on the lymphoproliferative response to HD
M and to phytohaemagglutinin in patients who never received HS, but ha
d no effect in patients receiving HS. We conclude that HS treatment se
ems to have an inhibiting effect upon this proliferative response, not
only inhibiting the degree of the allergen-induced lymphocyte prolife
ration, but also inhibiting the sensitivity of proliferating lymphocyt
es for IL-2. These inhibiting effects upon lymphocytic activation coul
d be responsible for the anti-inflammatory effects (i.e. suppression o
f the late asthmatic reaction) of HS.