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1
*
Thoracic Medicine, National Heart and Lung Institute, Imperial College School of Medicine, London, United Kingdom;
Thoracic Medicine, Chang Gung Memorial Hospital, Keelung, Taiwan, Republic of China; and
Department of Immunology, King’s College School of Medicine and Dentistry, London, United Kingdom
Th2 T cell immune-driven inflammation plays an important role in
allergic asthma. We studied the effect of counterbalancing Th1 T cells
in an asthma model in Brown Norway rats that favors Th2 responses. Rats
received i.v. transfers of syngeneic allergen-specific Th1 or Th2
cells, 24 h before aerosol exposure to allergen, and were studied
18–24 h later. Adoptive transfer of OVA-specific Th2 cells, but not
Th1 cells, and OVA, but not BSA exposure, induced bronchial
hyperresponsiveness (BHR) to acetylcholine and eosinophilia in a cell
number-dependent manner. Importantly, cotransfer of OVA-specific Th1
cells dose-dependently reversed BHR and bronchoalveolar lavage (BAL)
eosinophilia, but not mucosal eosinophilia. OVA-specific Th1 cells
transferred alone induced mucosal eosinophilia, but neither BHR nor BAL
eosinophilia. Th1 suppression of BHR and BAL eosinophilia was allergen
specific, since cotransfer of BSA-specific Th1 cells with the
OVA-specific Th2 cells was not inhibitory when OVA aerosol alone was
used, but was suppressive with OVA and BSA challenge. Furthermore,
recipients of Th1 cells alone had increased gene expression for IFN-
in the lungs, while those receiving Th2 cells alone showed increased
IL-4 mRNA. Importantly, induction of these Th2 cytokines was inhibited
in recipients of combined Th1 and Th2 cells. Anti-IFN- treatment
attenuated the down-regulatory effect of Th1 cells. Allergen-specific
Th1 cells down-regulate efferent Th2 cytokine-dependent BHR and BAL
eosinophilia in an asthma model via mechanisms that depend on IFN-.
Therapy designed to control the efferent phase of established asthma by
augmenting down-regulatory Th1 counterbalancing mechanisms should be
effective.
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