List of Titles

The NF-κB1 transcription factor prevents the intrathymic development of CD8 T cells with memory properties

- Gugasyan, Raffi, Horat, Elisha, Kinkel, Sarah, Ross, Fiona, Grigoriadis, George, Gray, Daniel, O'Keeffe, Meredith, Berzins, Stuart, Belz, Gabrielle, Grumont, Raelene, Banerjee, Ashish, Strasser, Andreas, Godfrey, Dale, Tsichlis, Phillip, Gerondakis, Steve

Authors: Gugasyan, Raffi , Horat, Elisha , Kinkel, Sarah , Ross, Fiona , Grigoriadis, George , Gray, Daniel , O'Keeffe, Meredith , Berzins, Stuart , Belz, Gabrielle , Grumont, Raelene , Banerjee, Ashish , Strasser, Andreas , Godfrey, Dale , Tsichlis, Phillip , Gerondakis, Steve
Date: 2012
Type: Text , Journal article
Relation: EMBO Journal Vol. 31, no. 3 (2012), p. 692-706
Full Text: false
Reviewed:
Description: The role of specific members of the NF-κB family of transcription factors in CD8 T-cell selection and development is largely unknown. Here, we show that mice lacking NF-κB1 develop a unique population of conventional CD8 single-positive (SP) thymocytes with memory T cell-like properties that populate peripheral immune organs. Development of this memory-like population is not due to PLZF + thymocytes and instead coincides with changes in CD8 T-cell selection. These include a reduction in the efficiency of negative selection and a dependence on MHC class Ia or Ib expressed by haematopoietic cells. These findings indicate that NF-κB1 regulates multiple events in the thymus that collectively inhibit the excess development of CD8 + thymocytes with memory cell characteristics. © 2012 European Molecular Biology Organization | All Rights Reserved.

Testing the NKT cell hypothesis in lenalidomide-treated myelodysplastic syndrome patients

- Chan, Angela, Neeson, Paul, Leeansyah, Edwin, Tainton, K., Quach, Hang, Prince, Henry, Godfrey, Dale, Ritchie, David, Berzins, Stuart

Authors: Chan, Angela , Neeson, Paul , Leeansyah, Edwin , Tainton, K. , Quach, Hang , Prince, Henry , Godfrey, Dale , Ritchie, David , Berzins, Stuart
Date: 2010
Type: Text , Journal article
Relation: Leukemia Vol. 24, no. 3 (2010), p. 592-600
Full Text: false
Reviewed:
Description: Myelodysplastic syndrome (MDS) comprises a group of clonal bone marrow disorders characterized by ineffective hematopoiesis and increased predisposition to acute myeloid leukemia. The causes of MDS remain poorly defined, but several studies have reported the NKT cell compartment of patients with MDS is deficient in number and functionally defective. In support of a central role for NKT cells, a pilot clinical study reported that lenalidomide (an approved treatment for MDS) increased NKT cell numbers in patients with MDS, and several in vitro studies showed lenalidomide specifically promoted NKT cell proliferation and cytokine production. We tested this in a much larger study and confirm a moderate in vitro augmentation of some NKT cell functions by lenalidomide, but find no impact on the NKT cell compartment of patients treated with lenalidomide, despite a consistently positive clinical response. We further show that the frequency and cytokine production of NKT cells is normal in patients with MDS before treatment and remains stable throughout 10 months of lenalidomide therapy. Collectively, our data challenge the concept that NKT cell defects contribute to the development of MDS, and show that a clinical response to lenalidomide is not dependent on modulation of NKT cell frequency or function. © 2010 Macmillan Publishers Limited All rights reserved.

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