MICE LACKING CD8-CELLS DEVELOP GREATER NUMBERS OF IGA-PRODUCING CELLSIN RESPONSE TO A RESPIRATORY VIRUS-INFECTION( T)

Antibody production profiles have been compared for Sendai virus infec tion of normal mice and mice that lack CD8(+) T cells as a consequence of treatment with a lymphocyte subset-specific monoclonal antibody or homozygous disruption of the beta(2)-microglobulin (beta 2-m(-/-)) ge ne encoding the light chain of the class I major histocompatibility co mplex glycoprotein. Using the single-cell ELISPOT assay, we show a rel ative increase in IgA antibody forming cell (AFC) numbers in the media stinal lymph node (MLN), spleen, and bone marrow of the CD8-depleted m ice. This is reflected in higher serum IgA titers. Similarly, secondar y infection with a large dose of Sendai virus leads to greater prevale nce of virus-specific IgA AFCs as early as Day 5 postinfection in the beta 2-m(-/-) mice. Also, in primed beta 2-m(-/-) mice challenged with vaccinia constructs containing the genes for the hemagglutinin-neuram inidase (HN), nuclear protein, or the fusion protein of Sendai virus, the majority of the virus-specific AFCs in the MLN are specific for HN and secrete IgA. (C) 1994 Academic Press, Inc.