EFFECTS OF DEPLETION OF CELLS BEARING THE INTERLEUKIN-2 RECEPTOR ON IMMUNOGLOBULIN PRODUCTION AND ALLERGIC AIRWAY RESPONSES IN THE RAT

Lymphocytes, key cells in chronic inflammation, are increased in the a irways of asthmatics and have increased expression of the interleukin- 2 (IL-2) receptor, a sign of activation. We determined the effects of depleting cells bearing IL-2 receptors on immunoglobulin (ig) producti on, airway inflammation, and airway responses after antigen challenge of Brown Norway rats that were sensitized to ovalbumin (OA). Both cont rol and ART-18 (antirat IL-2 receptor) antibodies inhibited plasma spe cific IgE and the early (ER) and late (LR) airway responses to antigen when given from zero to 14 d after sensitization. When ART-18 was adm inistered from 4 to 14 d after sensitization and compared with control animals, it inhibited OA specific IgE production from Day 21 onward, but it increased total IgE and specific IgG. These changes followed a significant increase in blood CD4(+) lymphocytes (%) in ART-18-treated animals 14 d after sensitization. The same protocol of administration did not affect Ig levels at 14 d, but it decreased neutrophil influx into the lungs 8 h after antigen challenge without any effects on the ER and LR. Administration of ART-18 at the time of antigen challenge d id not affect the subsequent airway inflammation or the increased resp onsiveness to methacholine that occurs 32 h after antigen challenge. I n summary, depletion of IL-2-receptor-bearing cells affects lymphocyte subsets and immunoglobulin production and it decreases the influx of neutrophils into the lungs 8 h after OA challenge, but it does not sig nificantly inhibit the ER, LR, or increased airway responsiveness afte r antigen challenge.