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Release in the Lung But Not for the Differentiation of Viral-Reactive Th1-Type Lymphocytes1
Department of Pathology and Molecular Medicine and Division of Infectious Diseases, Centre for Gene Therapeutics, McMaster University, Hamilton, Ontario, Canada
We demonstrated that IL-12 was induced during primary or secondary
pulmonary adenoviral infection in wild-type (wt) mice. However,
cellular responses were not compromised in the lungs of
IL-12-/- mice. The level of IFN-
in the lung was
similar in wt and IL-12-/- mice during pulmonary viral
infection. Upon Ag stimulation in vitro, lymphocytes from draining
lymph nodes or spleen of infected IL-12-/- mice released
large amounts of IFN-, but not IL-4, which were comparable to those
released by wt lymphocytes. Furthermore, a predominantly IgG2a response
to adenoviral infection was unimpaired in IL-12-/- mice.
These significant anti-adenoviral Th1-type responses in
IL-12-/- mice led to an efficient clearance of
virus-infected cells in the lung. Whether IL-18 was involved in
IL-12-independent anti-adenoviral immune responses was
investigated. Abrogation of endogenous IL-18 by an Ab resulted in
diminished IFN- release and lymphocytic infiltrate in the lung
during adenoviral infection. Nevertheless, the development of
lymphocytes of the Th1 phenotype was unimpaired in the absence of both
IL-12 and IL-18. In contrast to their intact ability to mount
Th1-type responses to viral infection,
IL-12-/- mice suffered impaired Th1-type immune responses
to pulmonary mycobacterial infection. Our findings suggest that IL-12,
although induced, is not required for Th1-type responses to respiratory
viral infection, in contrast to mycobacterial infection. IL-18 is
required for the optimal release of IFN- in the lung during viral
infection, but is not required for the generation of virus-reactive
Th1-type lymphocytes. Th1 differentiation during respiratory adenoviral
infection may involve molecules different from IL-12 or
IL-18.
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