CD3+CD16+NK1.1+B220+ large granular lymphocytes arise from both alpha-beta TCR+CD4-CD8- and gamma-delta TCR+CD4-CD8- cells.
CD3+CD16+NK1.1+B220+ large granular lymphocytes arise from both alpha-beta TCR+CD4-CD8- and gamma-delta TCR+CD4-CD8- cells.
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DOI：
10.1084/jem.179.6.1957
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发表时间：
1994-06-01
期刊：
影响因子：
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通讯作者：
Koyasu S
中科院分区：
文献类型：
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作者：
Koyasu S
在没有其它刺激的情况下，用重组白细胞介素2（IL 2）培养CD 4-CD 8-双阴性（DN）小鼠胸腺细胞和脾细胞导致产生DN-CD 3/TCR+ CD 16 + NK 1.1 +B220+大颗粒淋巴细胞（LGL）。纯化的DN α-β TCR+胸腺细胞和脾细胞是CD 16 + IL 2 R α-IL 2 R β +NK1.1+B220-CD 5 high。这些细胞是独特的，因为它们表达通常相互排斥的CD 16和T细胞受体（TCR）。此外，它们还表达自然杀伤（NK）标记NK1.1。这些细胞与IL 2培养数天导致DN α-β TCR+ CD 16 +NK1.1+B220+ CD 5- LGL的产生，表明胸腺和脾脏中的DN α-β TCR+细胞是先前报道的DN LGL的前体。DN γ-δ TCR+ CD 16- NK1.1-B220-CD 5高胸腺细胞和脾细胞也产生DN γ-δ TCR+ CD 16 +NK1.1+B220+ CD 5- LGL，其如先前用DN α-β TCR+ LGL细胞所示，对NK敏感的YAC-1细胞具有细胞毒性。细胞毒性活性也通过CD 16或γ-δ TCR诱导。因此，DN α-β TCR+和DN γ-δ TCR+ LGL细胞在表型上与TCR-NK细胞相似。DN α-β TCR+胸腺细胞表达低水平的高亲和力免疫球蛋白E受体（Fc γ RI γ）分子的γ亚基，这是CD 16表达的一种重要组分。在用IL 2培养后，Fc γ RI γ表达大大增强，导致更高的CD 16表面表达。与DN α-β TCR+胸腺细胞相反，DN γ-δ TCR+胸腺细胞不表达可检测的CD 16或Fc β RI γ mRNA，但两者的表达通过与IL 2培养诱导，导致表面上的CD 16表达。尽管DN α-β TCR+和DN γ-δ TCR+ LGL上的CD 16分子仅与Fc ε RI γ同二聚体相关，但这些细胞上的TCR与Fc ε RI γ同二聚体和/或CD 3 zeta-Fc ε RI γ异二聚体相关。这些结果表明，Fc γ RI γ亚基是T谱系细胞部分中TCR的组分。
Cultivation of CD4-CD8- double negative (DN) mouse thymocytes and splenocytes with recombinant interleukin 2 (IL2) in the absence of other stimulation results in the generation of DN- CD3/TCR+CD16+NK1.1+B220+ large granular lymphocytes (LGL). Purified DN alpha-beta TCR+ thymocytes and splenocytes are CD16+IL2R alpha-IL2R beta+NK1.1+B220-CD5high. These cells are unique in that they express both CD16 and T cell receptor (TCR) which are usually mutually exclusive. In addition, they express the natural killer (NK) marker, NK1.1. Cultivation of these cells with IL2 for several days results in the generation of DN alpha-beta TCR+CD16+NK1.1+B220+CD5- LGL, suggesting that DN alpha-beta TCR+ cells in thymus and spleen are the precursors of the DN LGL reported previously. DN gamma-delta TCR+CD16- NK1.1-B220-CD5high thymocytes and splenocytes also give rise to DN gamma-delta TCR+CD16+NK1.1+B220+CD5- LGL which, as shown previously with DN alpha-beta TCR+ LGL cells, are cytotoxic against NK-sensitive YAC-1 cells. Cytotoxic activity is also induced through either CD16 or the gamma-delta TCR. DN alpha-beta TCR+ and DN gamma-delta TCR+ LGL cells are thus similar in phenotype to TCR- NK cells. DN alpha-beta TCR+ thymocytes express low levels of the gamma subunit of the high affinity immunoglobulin E receptor (Fc epsilon RI gamma) molecule, an essential component of CD16 expression. Fc epsilon RI gamma expression is greatly enhanced after cultivation with IL2, resulting in a higher surface expression of CD16. In contrast to DN alpha-beta TCR+ thymocytes, DN gamma-delta TCR+ thymocytes do not express detectable CD16 or Fc epsilon RI gamma mRNA but expression of both is induced by cultivation with IL2, leading to the expression of CD16 on the surface. Whereas CD16 molecules on both DN alpha-beta TCR+ and DN gamma-delta TCR+ LGL are associated with only Fc epsilon RI gamma homodimers, the TCR on these cells are associated with an Fc epsilon RI gamma homodimer and/or CD3 zeta-Fc epsilon RI gamma heterodimers. These results demonstrate that the Fc epsilon RI gamma subunit is a component of the TCR in a fraction of T lineage cells.