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RIII-Mediated Production of TNF-
Induces Immune Complex Alveolitis Independently of CXC Chemokine Generation1
Departments of
*
Clinical Immunology and
Functional Anatomy, Medical School Hannover, Hannover, Germany; and
Department of Molecular Oncology, General Surgery, Witten/Herdecke University, Wuppertal, Germany
We recently demonstrated a codominant role of C5aR and Fc
RIII in
the initiation of IgG immune complex-mediated inflammation in mice. In
this study, we investigated the relative contribution of FcRIII in
the generation of several cytokines during experimental
hypersensitivity pneumonitis/alveolitis in vivo. Induction of immune
complex-alveolitis in C57BL/6 mice resulted in strong accumulation of
neutrophils into the lung and enhanced chemotactic activity within
bronchoalveolar lavage fluid accompanied by an increased production of
the proinflammatory cytokines TNF-
and IL-1
as well as the
ELR-CXC chemokines macrophage inflammatory protein-2 (MIP-2) and
cytokine-induced neutrophil chemoattractant (KC).
FcRIII-deficient C57BL/6 mice (FcRIII-/-) showed a
marked reduction of the inflammatory response due to decreased
production of TNF-, IL-1, and MIP-2. Results obtained in C57BL/6
mice either lacking the TNF- class I receptor
(TNF-RI-/-) or treated with neutralizing
anti-TNF- mAb demonstrated an essential contribution of TNF-
for mediating IL-1 release, neutrophil influx, and hemorrhage.
Surprisingly, MIP-2 and KC chemokine levels remained largely
unaffected in TNF-RI-/- mice or after functional
inhibition of TNF-. These data suggest that in immune complex
alveolitis, the activation of FcRIII may induce divergent downstream
effector pathways with TNF- acting independently of CXC chemokines
to trigger the inflammatory response in C57BL/6
mice.
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