Interferon-gamma inducible protein (IP-10) expression is mediated by CD8(+) T cells and is regulated by CD4(+) T cells during the elicitation of contact of hypersensitivity
Interferon-gamma inducible protein (IP-10) expression is mediated by CD8(+) T cells and is regulated by CD4(+) T cells during the elicitation of contact of hypersensitivity
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DOI：
10.1111/1523-1747.ep12363337
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发表时间：
1996-09-01
影响因子：
6.5
通讯作者：
Fairchild, RL
中科院分区：
文献类型：
--
作者：
Abe, M;Kondo, T;Fairchild, RL
为了研究CD 4（+）和CD 8（+）T细胞在接触性超敏反应中的潜在作用，我们检测了T细胞依赖的促炎细胞因子基因在二硝基氟苯和恶唑酮反应中的表达。从激发的耳组织中分离全细胞RNA，并通过北方印迹和光密度分析来分析细胞因子基因表达水平。检测的白细胞介素1 β和三种趋化因子基因（IP-10、JE和RC）的表达依赖于用于致敏的半抗原剂量，并与免疫应答相关，即，致敏前抗体介导的CD 8（+）T细胞的耗竭导致半抗原攻击后IP-10表达的缺失，表明免疫CD 8（+）T细胞介导IP-10表达的能力，CD 4（+）T细胞的耗竭导致在接触敏感性诱发期间IP-10和RC表达的较高水平，提示CD 4（+）T细胞抑制这些促炎基因的表达。CD 4（+）T细胞的消耗导致较高程度的接触性超敏反应，而CD 8（+）T细胞的消耗导致较低程度的反应。CD 8（+）T细胞消耗的免疫细胞的转移导致低但可检测水平的IP-10表达，表明一些恶唑酮免疫CD 4（+）T细胞介导IP-10表达的能力，这些结果表明，在接触性超敏反应的诱导过程中，促炎细胞因子基因表达的差异诱导，其中IP-10的表达主要由免疫CD 8（+）T细胞介导，并由免疫CD 4（+）T细胞抑制。
To investigate the potential roles of CD4(+) and CD8(+) T cells during contact hypersensitivity, we examined the T-cell-dependent expression of proinflammatory cytokine genes in the responses to dinitrofluorobenzene and oxazolone, Whole cell RNA was isolated from challenged ear tissue and analyzed for level of cytokine gene expression by Northern blot and densitometry analysis. Expression of interleukin 1 beta and the three chemokine genes (IP-10, JE, and RC) examined was dependent on the hapten dose used for sensitization and correlated with the immune response, i.e., ear swelling, elicited, Antibody-mediated depletion of CD8(+) T cells before sensitization resulted in the absence of IP-10 expression following hapten challenge, indicating the ability of immune CD8(+) T cells to mediate IP-10 expression, Depletion of CD4(+) T cells resulted in higher levels of IP-10 and RC expression during elicitation of contact sensitivity, suggesting CD4(+) T cells inhibit the expression of these proinflammatory genes. Depletion of CD4(+) T cells resulted in contact hypersensitivity responses of higher magnitude and depletion of CD8(+) T cells resulted in responses of lower magnitude, Transfer of CD8(+) T-cell-depleted immune cells resulted in low, but detectable levels of IP-10 expression, indicating the ability of some oxazolone-immune CD4(+) T cells to mediate IP-10 expression, These results indicate the differential induction of proinflammatory cytokine gene expression during elicitation of contact hypersensitivity in which expression of IP-10 is primarily mediated by immune CD8(+) T cells and inhibited by immune CD4(+) T cells.