DRUG SUSCEPTIBILITY OF PCA IN WBB6F1-W W-V MICE/

Our previous study revealed that passive cutaneous anaphylaxis (PCA) c an be produced in congenitally mast cell-deficient WBB6F1-W/W-v (abbre viated as W/W-v) mice on sensitization with undiluted or slightly dilu ted allogeneic and xenogeneic antisera but not on sensitization with a llogeneic monoclonal immunoglobulin (Ig)E and IgG1 antibodies regardle ss of the antibody concentration [1]. In view of these findings, the p resent study was conducted to characterize PCA in this strain from its drug susceptibilities using mast cell-bearing WBB6F1-+/+ (abbreviated as +/+) and B6D2F1 mice as references. PCA in W/W-v mice mediated by a low dilution (1:4) of hyperimmune serum to bovine serum albumin of t he B6D2F1 mouse origin was markedly suppressed by CV-6209, an antagoni st of platelet-activating factor (PAF), but not by antihistamines such as cyproheptadine and oxatomide. In contrast, PCA in +/+ and B6D2F1 m ice mediated by a high dilution (1:128) of the anti-serum (virtually b y IgG1 antibody) was nearly completely suppressed by antihistamines bu t not by CV-6209. A remarkable difference between PCA in W/W-v and ref erence mice was also observed in the susceptibility to monoclonal anti -mouse granulocyte (Gr-l) antibody: PCB in W/W-v mice was potently sup pressed by the 1- to 3-day pretreatment with this antibody but that in references was not at all. Putting these present results together wit h the previous finding that anti-granulocyte antibody greatly reduces circulatory Gr-1(+) leukocytes, 1 to 3 days after the treatment [2], i t is highly probable that PCA in W/W-v mice mediated by some antibody isotypes other than IgE and IgG1 is produced by PAF mainly released fr om Gr-1(+) cells, while IgG1 antibody-mediated PCA in mast cell-bearin g reference mice is evoked by histamine derived from mast cells. PCA h omologous to that in W/W-v mice could also be produced in the referenc e mice on sensitization with undiluted or slightly diluted antiserum, when generalized blueing due to excess IgG1 antibody was removed by th e oxatomide treatment before the antigen challenge.