EFFECT OF ANTI-CD4 ANTIBODY TREATMENT ON INFLAMMATORY ARTHRITIS IN MRL-LPR/LPR MICE

被引:26
作者
GILKESON, GS
SPURNEY, R
COFFMAN, TM
KURLANDER, R
RUIZ, P
PISETSKY, DS
机构
[1] DURHAM VET ADM HOSP,MED RES SERV,DURHAM,NC
[2] DUKE UNIV,MED CTR,DIV NEPHROL,DURHAM,NC 27710
[3] DUKE UNIV,MED CTR,DIV HEMATOL & ONCOL,DURHAM,NC 27710
[4] UNIV MIAMI,DEPT PATHOL,MIAMI,FL 33152
来源
CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY | 1992年 / 64卷 / 02期
关键词
D O I
10.1016/0090-1229(92)90195-T
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
MRL- lpr lpr mice develop an inflammatory arthritis in association with other manifestations of autoimmunity. Although a variety of immune cell disturbances have been described in these mice, the relationship of these abnormalities to the pathogenesis of arthritis has not yet been determined; the role of T cells is especially unclear since synovial hypertrophy and joint erosions have been noted in some studies in the absence of a significant T cell infiltrate. Therefore, to determine if T cells are required for arthritis in MRL- lpr lpr mice, we evaluated the effects of prolonged treatment with a monoclonal anti-CD4 antibody. Knee joints from treated mice had markedly reduced arthritis compared to saline-treated control animals as measured by the degree of synovial hypertrophy and inflammation. Nephritis in these mice was concomitantly reduced. In contrast, rheumatoid factor levels were not affected by CD4+ cell depletion, despite significant effects on anti-DNA. These results indicate that in MRL- lpr lpr mice anti-CD4 therapy can inhibit arthritis, suggesting an important role of T cells in the pathogenesis of this lesion. © 1992.
引用
收藏
页码:166 / 172
页数:7
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