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Departments of
*
Microbiology and
Anatomy, Saga Medical School, Saga, Japan; and
Department of Environmental Toxicology, Faculty of Pharmaceutical Sciences, Teikyo University, Kanagawa, Japan
Adjuvant arthritis (AA) is an experimental model of autoimmune
disease in rats induced by immunization with Mycobacterium
tuberculosis (MT). Induction of AA in other species, including
mice, has been shown to be difficult. In the present study, we found
that AA could be induced in mice if the animals were treated with a mAb
(11B11 mAb) against IL-4. Histologically, the joints exhibited synovial
edema with infiltration of many neutrophils in the early phase of
inflammation. In its late phase, there were proliferation of synovium,
cell infiltrate in which mononuclear cells predominated, and
destruction of cartilage and subchondral bone. The joint inflammation
was passively transferred to normal syngeneic recipient mice with
lymphoid cells but not with sera from mice immunized with
MT followed by treatment with the anti-IL-4 Ab.
Delayed-type hypersensitivity (DTH) and proliferative responses
of lymphoid cells to purified protein derivative were markedly
augmented in 11B11 mAb-treated mice. Furthermore, the induction of
arthritis was associated with a marked decrease in IL-4 secretion but a
significant increase in IFN-
and IL-2 production. Thus, the
neutralization of IL-4 by an anti-IL-4 Ab appears to be required
for the induction of AA in mice.
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