IL-4 PRODUCING CD4(+) TCR-ALPHA-BETA(INT) LIVER LYMPHOCYTES - INFLUENCE OF THYMUS, BETA(2)-MICROGLOBULIN AND NK1.1 EXPRESSION
IL-4 PRODUCING CD4(+) TCR-ALPHA-BETA(INT) LIVER LYMPHOCYTES - INFLUENCE OF THYMUS, BETA(2)-MICROGLOBULIN AND NK1.1 EXPRESSION
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DOI：
10.1093/intimm/7.11.1729
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发表时间：
1995-11-01
影响因子：
4.4
通讯作者：
KAUFMANN, SHE
中科院分区：
文献类型：
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作者：
EMOTO, M;EMOTO, Y;KAUFMANN, SHE
本报告描述了非常规CD4（+）TCR αβ淋巴细胞的发育、表型和功能特征，在C57BL/6小鼠中，大多数表达中等强度TCR αβ（TCR αβ（int））的肝淋巴细胞是CD4（+）NK1.1（+）并表达高度限制的TCR V-β 曲目，以 V(beta)8 为主，V(beta)7 和 V(beta)2 也有一定贡献。虽然这些细胞表达 CD4 辅助受体，但它们存在于 H2-I A beta (A beta)(-/-) 基因破坏突变体中，但在 β(2)-微球蛋白 (beta(2)m)(-/-) 突变体小鼠中显着减少，因此是 B(2)m 依赖性的，表达 CD4(+)NK1.1(+) TCR α 的胸腺细胞 beta表型也是beta(2)m偶然的，表明这两个T淋巴细胞群是相关的。肝脏和胸腺中的CD4(+)NK1.1(+)TCR αβ淋巴细胞共享一些标记，例如LFA-1(+)、CD44(+)、CD5(+)、LECAM-1(-)和IL-2R α(-)。在无胸腺 nu/nu 小鼠中未检测到 CD4(+)NK1.1(+) TCR α beta(int) 肝淋巴细胞，我们得出结论，β(2)m 表达对于 CD4(+)NK1.1(+) TCR α beta(int) 肝淋巴细胞的发育至关重要，并且胸腺起着主要作用，CD4f TCR NK1.1（-）小鼠品系中也发现了αβ（int）肝淋巴细胞，但缺乏NK1.1标记，我们假设NK1.1分子是NK1.1（+）小鼠品系中CD4（+）TCR αβ（int）肝淋巴细胞的特征标记，尽管其表达对于其发育不是必需的，肝脏 来自 beta(2)m(+/-) 的淋巴细胞，但不是来自 beta 2m(-/-) 的淋巴细胞，小鼠是响应 CD3 或 TCR α beta 参与的有效 IL-4 产生者，并且通过抗 NK1.1 mAb 治疗，肝脏淋巴细胞产生的 IL-4 显着减少。我们得出结论，CD4(+)NK1.1(+) TCR α β(int) 肝淋巴细胞能够响应 TCR 刺激产生 IL-4。
The present report describes developmental, phenotypic and functional features of unconventional CD4(+) TCR alpha beta lymphocytes, In C57BL/6 mice, the majority of liver lymphocytes expressing intermediate intensity of TCR alpha beta (TCR alpha beta(int)) are CD4(+) NK1.1(+) and express a highly restricted TCR V-beta repertoire, dominated by V(beta)8 with some contribution by V(beta)7 and V(beta)2. Although these cells express the CD4 co-receptor, they are present in H2-I A beta (A beta)(-/-) gene disruption mutants but are markedly reduced in beta(2)-microglobulin (beta(2)m)(-/-) mutant mice and hence are B(2)m dependent, Thymocytes expressing the CD4(+)NK1.1(+) TCR alpha beta phenotype are also beta(2)m contingent, suggesting that these two T lymphocyte populations are related, The CD4(+)NK1.1(+)TCR alpha beta lymphocytes in liver and thymus share several markers such as LFA-1(+), CD44(+), CD5(+), LECAM-1(-) and IL-2R alpha(-). The CD4(+)NK1.1(+) TCR alpha beta(int) liver lymphocytes were not detected in athymic nu/nu mice, We conclude that beta(2)m expression is crucial for development of the CD4(+)NK1.1(+) TCR alpha beta(int) liver lymphocytes and that thymus plays a major role, CD4f TCR alpha beta(int) liver lymphocytes were also identified in NK1.1(-) mouse strains, there lacking the NK1.1 marker, We assume that the NK1.1 molecule is a characteristic marker of the CD4(+) TCR alpha beta(int) liver lymphocytes in NK1.1(+) mouse strains, although its expression is not obligatory for their development, The liver lymphocytes from beta(2)m(+/-), but not from beta 2m(-/-), mice are potent IL-4 producers in response to CD3 or TCR alpha beta engagement and the IL-4 production by liver lymphocytes was markedly reduced by treatment with anti-NK1.1 mAb, We conclude that the CD4(+)NK1.1(+) TCR alpha beta(int) liver lymphocytes are capable of producing IL-4 in response to TCR stimulation.