Abstract
In mice, the transcription factor, PLZF, controls the development of effector functions in invariant NKT cells and a subset of NKT cell-like, γδ T cells. Here, we show that in human lymphocytes, in addition to invariant NKT cells, PLZF was also expressed in a large percentage of CD8+ and CD4+ T cells. Furthermore, PLZF was also found to be expressed in all γδ T cells and in all NK cells. Importantly, we show that in a donor lacking functional PLZF, all of these various lymphocyte populations were altered. Therefore, in contrast to mice, PLZF appears to control the development and/or function of a wide variety of human lymphocytes that represent more than 10% of the total PBMCs. Interestingly, the PLZF-expressing CD8+ T cell population was found to be expanded in the peripheral blood of patients with metastatic melanoma but was greatly diminished in patients with autoimmune disease.
Highlights
The promyelocytic leukemia zinc finger (PLZF, ZBTB16) transcriptional regulator is a member of the BTB/POZ-ZF (Broad complex, tramtrack, bric-a-brac or poxvirus and zinc finger-zinc finger; BTB-ZF) family of proteins that have a wide variety of biological activities [1]
The cd TCR and invariant natural killer T (iNKT) cell-negative, CD3+ T-cell compartment can be demarcated by the expression of CD161 and CD56
We show that in people, CD8+ and CD4+ CD161hi T cells, all cd T cells, NKT cells and all NK cells express PLZF
Summary
The promyelocytic leukemia zinc finger (PLZF, ZBTB16) transcriptional regulator is a member of the BTB/POZ-ZF (Broad complex, tramtrack, bric-a-brac or poxvirus and zinc finger-zinc finger; BTB-ZF) family of proteins that have a wide variety of biological activities [1]. Over the last few years, it has become apparent that BTB-ZF proteins are critical regulators of immune system development and function. Bcl has been shown to be necessary for both the B cell germinal center reaction [2,3] as well as for the development of follicular helper T cells [4,5]. ThPok has been shown to be necessary and sufficient for CD4 T cell development [6] and the B cell versus T cell commitment step is controlled by LRF (leukemia/lymphoma related factor) [7]. Mazr influences CD8 T cell development, in part by regulating the expression of ThPok [8]. The fusion protein that results from this translocation was subsequently shown to be an important determining factor in the development
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