Airway hyperresponsiveness (AHR) is a hallmark of asthma(1) and a heri
table polygenic trait in the mouse(2). In the mouse, candidate gene pr
oducts of hematopoietic origin implicated in asthma mapped to the regi
ons of the previously defined quantitative trait loci(2). Since hemato
poietic cells(3-5) have been implicated in the pathogenesis of asthma,
we evaluated the role of hematopoietic cells in general and T cells s
pecifically in the genetic modulation of native airway responsiveness
in mice. Here, with the use of bone marrow transplantation, anti-T-cel
l monoclonal antibody treatment and T-cell transfer, we demonstrate th
at intrinsic non-atopic AHR is mediated by T lymphocytes. Our data sup
port the novel concept that, in the absence of identified environmenta
l influences, T cells enhance genetically determined airway responsive
ness.