scholarly journals Changes in bone marrow innate lymphoid cell subsets in monoclonal gammopathy: target for IMiD therapy

2017 ◽  
Vol 1 (25) ◽  
pp. 2343-2347 ◽  
Author(s):  
Jithendra Kini Bailur ◽  
Sameet Mehta ◽  
Lin Zhang ◽  
Natalia Neparidze ◽  
Terri Parker ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Lymphoid Cell ◽  
Monoclonal Gammopathy ◽  
Cell Function ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Innate Lymphoid Cell ◽  
Key Points ◽  
And Function

Key Points Altered number, subset composition, and function of bone marrow innate lymphoid cells are early events in monoclonal gammopathies. Pomalidomide therapy leads to reduction in Ikzf1 and Ikzf3 and enhanced human innate lymphoid cell function in vivo.

scholarly journals The Role of TOX in the Development of Innate Lymphoid Cells

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Corey R. Seehus ◽  
Jonathan Kaye
Keyword(s):  
Bone Marrow ◽  
Immune System ◽  
Natural Killer ◽  
Cell Fate ◽  
Lymphoid Cell ◽  
Adaptive Immune System ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Innate Lymphoid Cell

TOX, an evolutionarily conserved member of the HMG-box family of proteins, is essential for the development of various cells of both the innate and adaptive immune system. TOX is required for the development of CD4+T lineage cells in the thymus, including natural killer T and T regulatory cells, as well as development of natural killer cells and fetal lymphoid tissue inducer cells, the latter required for lymph node organogenesis. Recently, we have identified a broader role for TOX in the innate immune system, demonstrating that this nuclear protein is required for generation of bone marrow progenitors that have potential to give rise to all innate lymphoid cells. Innate lymphoid cells, classified according to transcription factor expression and cytokine secretion profiles, derive from common lymphoid progenitors in the bone marrow and require Notch signals for their development. We discuss here the role of TOX in specifying CLP toward an innate lymphoid cell fate and hypothesize a possible role for TOX in regulating Notch gene targets during innate lymphoid cell development.

scholarly journals Activation of group 2 innate lymphoid cells alleviates aging-associated cognitive decline

2020 ◽  
Vol 217 (4) ◽  
Author(s):  
Ivan Ting Hin Fung ◽  
Poornima Sankar ◽  
Yuanyue Zhang ◽  
Lisa S. Robison ◽  
Xiuli Zhao ◽  
...  
Keyword(s):  
Cognitive Decline ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Brain Physiology ◽  
Aged Brain ◽  
Group 2 ◽  
Resident Group ◽  
And Function

Increasing evidence has challenged the traditional view about the immune privilege of the brain, but the precise roles of immune cells in regulating brain physiology and function remain poorly understood. Here, we report that tissue-resident group 2 innate lymphoid cells (ILC2) accumulate in the choroid plexus of aged brains. ILC2 in the aged brain are long-lived, are relatively resistant to cellular senescence and exhaustion, and are capable of switching between cell cycle dormancy and proliferation. They are functionally quiescent at homeostasis but can be activated by IL-33 to produce large amounts of type 2 cytokines and other effector molecules in vitro and in vivo. Intracerebroventricular transfer of activated ILC2 revitalized the aged brain and enhanced the cognitive function of aged mice. Administration of IL-5, a major ILC2 product, was sufficient to repress aging-associated neuroinflammation and alleviate aging-associated cognitive decline. Targeting ILC2 in the aged brain may provide new avenues to combat aging-associated neurodegenerative disorders.

scholarly journals Atorvastatin enhances bone marrow endothelial cell function in corticosteroid-resistant immune thrombocytopenia patients

Blood ◽  
2018 ◽  
Vol 131 (11) ◽  
pp. 1219-1233 ◽  
Author(s):  
Yuan Kong ◽  
Xie-Na Cao ◽  
Xiao-Hui Zhang ◽  
Min-Min Shi ◽  
Yue-Yun Lai ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Endothelial Cell ◽  
Immune Thrombocytopenia ◽  
Cell Function ◽  
Novel Therapy ◽  
Endothelial Cell Function ◽  
Therapy Approach ◽  
Key Points ◽  
Bone Marrow Endothelial Cell ◽  
And Function

Key Points Impaired BM EPCs were found in corticosteroid-resistant ITP patients. Atorvastatin improved BM EPC quantity and function, representing a novel therapy approach for corticosteroid-resistant ITP patients.

scholarly journals G9a regulates group 2 innate lymphoid cell development by repressing the group 3 innate lymphoid cell program

2016 ◽  
Vol 213 (7) ◽  
pp. 1153-1162 ◽  
Author(s):  
Frann Antignano ◽  
Mitchell Braam ◽  
Michael R. Hughes ◽  
Alistair L. Chenery ◽  
Kyle Burrows ◽  
...  
Keyword(s):  
Lymphoid Cell ◽  
Lymphoid Cells ◽  
Innate Lymphoid Cell ◽  
Genome Wide ◽  
Allergic Lung Inflammation ◽  
Severe Reduction ◽  
Repressive Histone Mark ◽  
Lysine Methyltransferase ◽  
Group 2 ◽  
And Function

Innate lymphoid cells (ILCs) are emerging as important regulators of homeostatic and disease-associated immune processes. Despite recent advances in defining the molecular pathways that control development and function of ILCs, the epigenetic mechanisms that regulate ILC biology are unknown. Here, we identify a role for the lysine methyltransferase G9a in regulating ILC2 development and function. Mice with a hematopoietic cell–specific deletion of G9a (Vav.G9a−/− mice) have a severe reduction in ILC2s in peripheral sites, associated with impaired development of immature ILC2s in the bone marrow. Accordingly, Vav.G9a−/− mice are resistant to the development of allergic lung inflammation. G9a-dependent dimethylation of histone 3 lysine 9 (H3K9me2) is a repressive histone mark that is associated with gene silencing. Genome-wide expression analysis demonstrated that the absence of G9a led to increased expression of ILC3-associated genes in developing ILC2 populations. Further, we found high levels of G9a-dependent H3K9me2 at ILC3-specific genetic loci, demonstrating that G9a-mediated repression of ILC3-associated genes is critical for the optimal development of ILC2s. Together, these results provide the first identification of an epigenetic regulatory mechanism in ILC development and function.

scholarly journals In vivo stem cell function of interleukin-3-induced blast cells

Blood ◽  
1991 ◽  
Vol 78 (2) ◽  
pp. 318-322
Author(s):  
J Tsunoda ◽  
S Okada ◽  
J Suda ◽  
K Nagayoshi ◽  
H Nakauchi ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Hematopoietic Stem Cells ◽  
Cell Function ◽  
Lymphoid Cells ◽  
Hematopoietic Stem ◽  
Interleukin 3 ◽  
Donor Cells ◽  
Blast Cells

The treatment of mice with high doses of 5-fluorouracil (5-FU) results in an enrichment of primitive hematopoietic progenitors. Using this procedure, we obtained a new class of murine hematopoietic colonies that had very high secondary plating efficiencies in vitro and could differentiate into not only myeloid cells but also into lymphoid lineage cells. The phenotypes of interleukin-3 (IL-3) induced blast colony cells were Thy-1-positive and lineage-marker-negative. We examined whether these blast colony cells contained primitive hematopoietic stem cells in vivo and could reconstitute hematopoietic tissues in lethally irradiated mice. Blast colony cells could generate macroscopic visible spleen colonies on days 8 and 12, and 5 x 10(3) blast cells were sufficient to protect them from lethally irradiation. It was shown that 6 or 8 weeks after transplantation of 5 x 10(3) blast cells, donor male cells were detected in the spleen and thymus of the female recipients but not in the bone marrow by Southern blot analysis using Y-encoded DNA probe. After 10 weeks, bone marrow cells were partially repopulated from donor cells. In a congenic mouse system, donor-derived cells (Ly5.2) were detected in the thymus and spleen 6 weeks after transplantation. Fluorescence-activated cell sorter analyses showed that B cells and macrophages developed from donor cells in the spleen. In the thymus, donor-derived cells were found in CD4, CD8 double-positive, single-positive, and double-negative populations. Reconstitution of bone marrow was delayed and myeloid and lymphoid cells were detected 10 weeks after transplantation. These results indicate that IL-3-induced blast cells contain the primitive hematopoietic stem cells capable of reconstituting hematopoietic organs in lethally irradiated mice.

scholarly journals The development of innate lymphoid cells requires TOX-dependent generation of a common innate lymphoid cell progenitor

2015 ◽  
Vol 16 (6) ◽  
pp. 599-608 ◽  
Author(s):  
Corey R Seehus ◽  
Parinaz Aliahmad ◽  
Brian de la Torre ◽  
Iliyan D Iliev ◽  
Lindsay Spurka ◽  
...  
Keyword(s):  
Lymphoid Cell ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Innate Lymphoid Cell

scholarly journals Loss of thymic innate lymphoid cells leads to impaired thymopoiesis in experimental graft-versus-host disease

Blood ◽  
2017 ◽  
Vol 130 (7) ◽  
pp. 933-942 ◽  
Author(s):  
Jarrod A. Dudakov ◽  
Anna M. Mertelsmann ◽  
Margaret H. O’Connor ◽  
Robert R. Jenq ◽  
Enrico Velardi ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Transplant ◽  
Graft Versus Host Disease ◽  
Marrow Transplant ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Allogeneic Bone ◽  
Epithelial Damage ◽  
Graft Versus Host ◽  
Key Points

Key Points Thymic ILCs and their production of IL-22 are reduced in mice with GVHD; IL-22 deficiency worsens thymic epithelial damage in GVHD. Administration of IL-22 posttransplant can enhance thymopoiesis after experimental allogeneic bone marrow transplant.

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