B6/lpr小鼠中巨噬细胞与缺陷性迟发型超敏反应的关系。
Relationship of macrophages to defective delayed-type hypersensitivity in B6/lpr mice.
作者信息
Okuyama H, Yamamoto K, Matsunaga T, Kobayashi S, Hashimoto Y
出版信息
Clin Exp Immunol. 1986 Dec;66(3):599-605.
These experiments were undertaken to clarify whether or not suppressor macrophages contribute to deficiency of delayed-type hypersensitivity induced by BCG CW immunization in B6/lpr mice. Addition of indomethacin in vitro did not increase MIF production by immunized lpr lymph node cells. Adherent cells in lymph node cell suspensions from lpr mice did not interfere with MIF production by nonadherent lymph node cells from immunized B6 mice. On the other hand, MIF production by nonadherent lymph node cells from immunized B6/lpr mice was not restored even if they were cultured with adherent lymph node cells from immunized B6 mice. In addition, macrophages from nonimmunized B6/lpr mice showed normal reactivity to MIF when lymphocytes coexisting with the macrophages in large proportions were depleted from PEC. These results suggest that macrophages make no contribution to the deficiency of DTH expression of B6/lpr mice.
进行这些实验是为了阐明抑制性巨噬细胞是否导致B6/lpr小鼠中卡介苗细胞壁（BCG CW）免疫诱导的迟发型超敏反应缺陷。体外添加吲哚美辛不会增加免疫的lpr淋巴结细胞产生巨噬细胞移动抑制因子（MIF）。来自lpr小鼠的淋巴结细胞悬液中的贴壁细胞不会干扰来自免疫的B6小鼠的非贴壁淋巴结细胞产生MIF。另一方面，即使将来自免疫的B6/lpr小鼠的非贴壁淋巴结细胞与来自免疫的B6小鼠的贴壁淋巴结细胞一起培养，其产生MIF的能力也无法恢复。此外，当从腹腔渗出细胞（PEC）中大量去除与巨噬细胞共存的淋巴细胞时，来自未免疫的B6/lpr小鼠的巨噬细胞对MIF表现出正常反应。这些结果表明巨噬细胞对B6/lpr小鼠迟发型超敏反应表达缺陷没有作用。
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