We have tested the hypothesis that exposure to ultraviolet light would inhi
bit T helper-1 (Th1) responses and stimulate T helper-2 (Th2) responses, an
d that thus in a mouse model of allergic (i.e. extrinsic) asthma (using ova
lbumin [OVA] as the allergen) increased symptoms would he observed, while i
n a model of Th1-dependent occupational asthma lin which picryl chloride is
the allergen) decreased symptoms would be observed. Whereas reduced interf
eron (IFN)-gamma production, decreased inflammatory responses in the airway
s, and reduced airway reactivity to nonspecific stimuli were observed in UV
-preexposed picryl chloride sensitized and challenged mice, the results in
the OVA model were less clear. Increased interleukin (IL)-10 production as
a result of UV exposure was observed, together with unchanged IL-4 and IFN-
gamma. In addition, decreased OVA-specific immunoglobin, IgG1 and IgE, tite
rs were noted, as well as decreased nonspecific airway hyperreactivity, Eos
inophilic inflammatory responses were not influenced. The results indicate
that UV exposure can have systemic effects that influence ongoing immune re
sponses ill the respiratory tract. The effects are not only restricted to i
mmune responses that are predominantly Th1 dependent (i.e. pulmonary delaye
d-type hypersensitivity and IFN-gamma production in response to picryl chlo
ride) but also to immune response that are predominantly Th2 dependent, i.e
. decreased specific IgE titers.