MICE LACKING CD8+ T-CELLS DEVELOP GREATER NUMBERS OF IGA-PRODUCING CELLS IN RESPONSE TO A RESPIRATORY VIRUS-INFECTION

Antibody production profiles have been compared for Sendai virus infection 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(-/-)) gene encoding the light chain of the class I major histocompatibility complex glycoprotein. Using the single-cell ELISPOT assay, we show a relative increase in IgA antibody forming cell (AFC) numbers in the mediastinal lymph node (MLN), spleen, and bone marrow of the CD8-depleted mice. This is reflected in higher serum IgA titers. Similarly, secondary infection with a large dose of Sendai virus leads to greater prevalence 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-neuraminidase (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.