Immunoglobulin classes which induce a non-immediate asthmatic response (non-IAR) in the case of low level of IgE antibody are still unknown, although IAR is mediated by IgE. To elucidate the relationship between antibodies and late asthmatic responses (LAR), antigen-specific IgG subclass antibodies in the serum and bronchoalveolar lavage fluid (BALF) of asthmatics were measured by avidin-biotin ELISA before provocation by antigen. The BALF levels of IgG and IgG1 antibodies to mite and Candida antigen in bronchial asthmatics were higher than those in healthy subjects (p<0.05). Followed by inhalation of house dust or Candida antigen, bronchial asthmatics were divided into group A (higher levels of BALF IgG1 antibody) and gourp B (lower levels of BALF IgG1 antibody). The percentages of LAR including DAR after inhalation of house dust antigen in group A were significantly higher than those in group B (p<0.05). The percentages of LAR including DAR after inhalation of Candida antigen in group A were significantly higher than those in group B (p<0.01). In asthmatics with LAR after inhalation of house dust antigen or Candida antigen, the BALF levels of antigen-specific IgG and IgG1 antibodies were significantly higher than those in asthmatics without LAR of healthy subjects (p<0.01). In asthmatics with LAR after inhalation of house dust antigen or Candida antigen, the BALF levels of antigen-specific IgG and IgG1 antibodies were significantly higher than those in asthmatics without LAR of healthy subjects (p<0.01). In asthmatics with LAR, the relative (to albumin) of coefficients of excretion (RCE) in the BALF of antigen-specific IgG and IgG1 antibodies were higher than those in asthmatics without LAR of healthy subjects. These findings suggest that local production of antigen-specific IgG and IgG1 antibodies incerases in asthmatics with LAR, and that these antibodies may induce LAR.