MHC-recognizing receptors: they're not just for T cells anymore.
MHC-recognizing receptors: they're not just for T cells anymore.
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MHC 识别受体：它们不再仅适用于 T 细胞。
DOI：
10.1016/1074-7613(95)90153-1
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发表时间：
1995
期刊：
影响因子：
32.4
通讯作者：
P. Leibson
中科院分区：
文献类型：
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作者：
P. Leibson
自然杀伤（NK）细胞是淋巴细胞的亚群，其可以介导某些肿瘤细胞、病毒感染的细胞和正常造血细胞的溶解（Trinchieri，1989）。然而，很少有人知道有关受体启动的机制，调节这些激活。事实上，一些违反直觉的观察结果一直困扰着对它们的生物学感兴趣的研究人员。例如，为什么来自F1杂交小鼠的NK细胞排斥来自任一亲本品系的骨髓细胞（杂交抗性）？更广泛地说，为什么NK细胞优先杀死缺乏主要组织相容性复合体（MHC）I类分子的靶细胞？这篇评论的重点是最近的调查，提供了新的见解调节这些过程的机制。具体地，分析已经鉴定了NK细胞克隆群体上的新型MHC识别受体，并且似乎在这些受体结合其配体后产生的负调节信号严重影响其细胞功能。杂交抗性和“缺失的Selr”几十年前，研究人员清楚地确定，两个H-2不同鼠亲本之间的F1杂交体排斥来自任一亲本的骨髓细胞移植物（Snell，1958年; Cudkowicz和Stimpfling，1984年; Yu等人，1992年）。这种杂交抗性与显性遗传对T细胞介导的移植物排斥的易感性不一致，并产生了解释这种差异的新模型。随后的研究表明NK细胞介导这种杂交抗性（Kiessling et al.，1977），更一般地说，NK细胞可以消除细胞，因为关键的MHC I类分子不存在于靶细胞表面（Ljunggren和Karre，1990）。这包括清楚的体内证明，NK细胞可以介导MHC I类缺陷型骨髓细胞的排斥（例如，在正常MHC表达小鼠中排斥的f32-微球蛋白缺陷型骨髓细胞）（Bix等人，1991; Hoglund等人，1991）和MHC I类缺陷型肿瘤细胞（例如，在同基因小鼠中被排斥的H-2 I类缺陷型变异淋巴瘤）（Karre等，1988年）。甚至表达MHC I类转基因的小鼠也可以排斥除了不存在转基因之外在MHC表达方面相同的肿瘤细胞（Hoglund等人，1988年）。靶细胞对NK细胞介导的细胞毒性的易感性与自身I类细胞的表达之间的负相关性导致了一种提出的模型，其中NK细胞上的新型受体对MHC的识别产生负信号，该负信号下调NK细胞对I类+靶细胞的杀伤（效应抑制模型）（Ljunggren和Karre，1990）。
Natural killer (NK) cells are a subpopulation of lymphocytes that can mediate the lysis of certain tumor ceils, virus-infected cells, and normal hematopoietic cells (Trinchieri, 1989). Yet, little has been known regarding the receptor-initiated mechanisms regulating these activations. In fact, several counterintuitive observations have dogged investigators interested in their biology. For example, why do NK cells from Fl hybrid mice reject bone marrow cells derived from either parental strain (hybrid resistance)? More broadly, why do NKcells preferentially kill target cells lacking major histocompatibility complex (MHC) class I molecules? This review focuses on recent investigations that have provided new insights into the mechanisms regulating these processes. Specifically, analyses have identified novel MHC-recognizing receptors on clonal populations of NK cells, and it appears that the negative regulatory signals generated after these receptors bind their ligands critically influences their cellular functions.Hybrid Resistance and the “Missing Selr Decades ago, investigators clearly established that an Fl hybrid between two H-2 disparate murine parents rejects bone marrow cell grafts from either parent (Snell, 1958; Cudkowicz and Stimpfling, 1984; Yu et al., 1992). This hybrid resistance was inconsistent with dominantly inherited susceptibility to T cell-mediated graft rejection, and novel models to explain this discrepancy were generated. Subsequent studies showed that NK cells mediated this hybrid resistance (Kiessling et al., 1977) and, moregenerally, that NK cells can eliminate cells because critical MHC class I molecules are absent from the cell surface of the target (Ljunggren and Karre, 1990). This included clear in vivo demonstrations that NK cells can mediate rejection of MHC class l-deficient bone marrow cells (eg, f32-microglobulin-deficient bone marrow cells rejected in normal MHC-expressing mice)(Bix et al., 1991; Hoglund et al., 1991) and MHC class l-deficient tumor cells (eg, H-2 class l-deficient variant lymphomas rejected in syngeneic mice)(Karre et al., 1988). Even mice expressing an MHC class I transgene could reject tumor cells identical in MHC expression except for the absence of the transgene (Hoglund et al., 1988). The inverse correlation between the susceptibility of target cells to NK cell-mediated cytotoxic-ity and the expression of self-class I led to a proposed model in which MHC recognition by novel receptors on NK cells results in a negative signal that down-modulates NK cell killing of class I+ targets (effector inhibition model)(Ljunggren and Karre, 1990).
肿瘤靶标上的 MHC I 类表达可抑制自然杀伤细胞介导的细胞毒性，而不干扰靶标识别。
DOI：
--
发表时间：
1993
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Kaufman,DS;Schoon,RA;Leibson,PJ
通讯作者：
Leibson,PJ
影响因子：
56.9
作者：
PHILLIPS, JH;GUMPERZ, JE;LANIER, LL
通讯作者：
LANIER, LL
肽诱导调节靶细胞对自然杀伤的敏感性。
DOI：
--
发表时间：
1992
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Storkus,WJ;Salter,RD;Cresswell,P;Dawson,JR
通讯作者：
Dawson,JR