期刊
JOURNAL OF IMMUNOLOGY
卷 167, 期 5, 页码 2985-2990出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.167.5.2985
关键词
-
类别
资金
- NIAID NIH HHS [AI38339, AI07019] Funding Source: Medline
- NIAMS NIH HHS [P30AR41942, AR44077] Funding Source: Medline
When mutations that inactivate molecules that function in the immune system have been crossed to murine lupus strains, the result has generally been a uniform up-regulation or down-regulation of autoimmune disease in the end organs. In the current work we report an interesting dissociation of target organ disease in beta (2)-microglobulin (beta (2)m)-deficient MRL-Fas(lpr) (MRL/lpr) mice: lupus; skin lesions are accelerated, whereas nephritis is ameliorated. beta (2)m deficiency affects the expression of classical and nonclassical MHC molecules and thus prevents the normal development of CD8- as well as CD1-dependent NK1(+) T cells. To further define the mechanism by which beta (2)m deficiency accelerates skin disease, we studied CD1-deficient MRL/lpr mice. These mice do not have accelerated skin disease, excluding a CD1 or NK1(+) T cell-dependent mechanism of beta (2)m deficiency. The data indicate that the regulation of systemic disease is not solely governed by regulation of initial activation of autoreactive lymphocytes in secondary lymphoid tissue, as this is equally relevant to renal and skin diseases. Rather, regulation of autoimmunity can also occur at the target organ level, explaining the divergence of disease in skin and kidney in beta (2)m-deficient mice.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据