scholarly journals High-frequency and activation of CD4+CD25+ T cells maintain persistent immunotolerance induced by congenital ALV-J infection

2021 ◽  
Vol 52 (1) ◽  
Author(s):  
Shuhai He ◽  
Gaoying Zheng ◽  
Defang Zhou ◽  
Li Huang ◽  
Jianguo Dong ◽  
...  
Keyword(s):  
T Cells ◽  
B Cells ◽  
High Frequency ◽  
Marginal Zone ◽  
Congenital Infection ◽  
Underlying Mechanism ◽  
Mrna Levels ◽  
Immune Organs ◽  
Surface Receptor ◽  
Avian Leukosis Virus Subgroup

AbstractCongenital avian leukosis virus subgroup J (ALV-J) infection can induce persistent immunotolerance in chicken, however, the underlying mechanism remains unclear. Here, we demonstrate that congenital ALV-J infection induces the production of high-frequency and activated CD4+CD25+ Tregs that maintain persistent immunotolerance. A model of congenital infection by ALV-J was established in fertilized eggs, and hatched chicks showed persistent immunotolerance characterized by persistent viremia, immune organ dysplasia, severe imbalance of the ratio of CD4+/CD8+ T cells in blood and immune organs, and significant decrease in CD3+ T cells and Bu-1+ B cells in the spleen. Concurrently, the mRNA levels of IL-2, IL-10, and IFN-γ showed significant fluctuations in immune organs. Moreover, the frequency of CD4+CD25+ Tregs in blood and immune organs significantly increased, and the frequency of CD4+CD25+ Tregs was positively correlated with changes in ALV-J load in immune organs. Interestingly, CD4+CD25+ Tregs increased in the marginal zone of splenic nodules in ALV-J-infected chickens and dispersed to the germinal center. In addition, the proliferation and activation of B cells in splenic nodules was inhibited, and the number of IgM+ and IgG+ cells in the marginal zone significantly decreased. We further found that the mRNA levels of TGF- β and CTLA-4 in CD4+CD25+ Tregs of ALV-J-infected chickens significantly increased. Together, high-frequency and activated CD4+CD25+ Tregs inhibited B cells functions by expressing the inhibitory cytokine TGF-β and inhibitory surface receptor CTLA-4, thereby maintaining persistent immunotolerance in congenital ALV-J-infected chickens.

scholarly journals WASP confers selective advantage for specific hematopoietic cell populations and serves a unique role in marginal zone B-cell homeostasis and function

Blood ◽  
2008 ◽  
Vol 112 (10) ◽  
pp. 4139-4147 ◽  
Author(s):  
Lisa S. Westerberg ◽  
Miguel A. de la Fuente ◽  
Fredrik Wermeling ◽  
Hans D. Ochs ◽  
Mikael C. I. Karlsson ◽  
...  
Keyword(s):  
T Cells ◽  
B Cells ◽  
B Cell ◽  
Marginal Zone ◽  
Hematopoietic Cells ◽  
Selective Advantage ◽  
Relative Contribution ◽  
B Cell Homeostasis ◽  
And Function

Abstract Development of hematopoietic cells depends on a dynamic actin cytoskeleton. Here we demonstrate that expression of the cytoskeletal regulator WASP, mutated in the Wiskott-Aldrich syndrome, provides selective advantage for the development of naturally occurring regulatory T cells, natural killer T cells, CD4+ and CD8+ T lymphocytes, marginal zone (MZ) B cells, MZ macrophages, and platelets. To define the relative contribution of MZ B cells and MZ macrophages for MZ development, we generated wild-type and WASP-deficient bone marrow chimeric mice, with full restoration of the MZ. However, even in the presence of MZ macrophages, only 10% of MZ B cells were of WASP-deficient origin. We show that WASP-deficient MZ B cells hyperproliferate in vivo and fail to respond to sphingosine-1-phosphate, a crucial chemoattractant for MZ B-cell positioning. Abnormalities of the MZ compartment in WASP−/− mice lead to aberrant uptake of Staphylococcus aureus and to a reduced immune response to TNP-Ficoll. Moreover, WASP-deficient mice have increased levels of “natural” IgM antibodies. Our findings reveal that WASP regulates both development and function of hematopoietic cells. We demonstrate that WASP deficiency leads to an aberrant MZ that may affect responses to blood-borne pathogens and peripheral B-cell tolerance.

Terminal plasmocytoid differentiation of malignant B cells induced by autotumor-reactive CD4+ T cells in one case of splenic marginal zone B-cell lymphoma

Blood ◽  
2002 ◽  
Vol 99 (1) ◽  
pp. 388-390 ◽  
Author(s):  
Thierry Bonnefoix ◽  
Jian-Qing Mi ◽  
Pascal Perron ◽  
Mary Callanan ◽  
Cosima Semoun ◽  
...  
Keyword(s):  
T Cells ◽  
B Cells ◽  
B Cell ◽  
Cd4 T Cells ◽  
Marginal Zone ◽  
Cell Lymphoma ◽  
B Cell Lymphoma

scholarly journals Resident enteric microbiota and CD8+ T cells shape the abundance of marginal zone B cells

2008 ◽  
Vol 38 (12) ◽  
pp. 3411-3425 ◽  
Author(s):  
Bo Wei ◽  
Thomas T. Su ◽  
Harnisha Dalwadi ◽  
Robert P. Stephan ◽  
Daisuke Fujiwara ◽  
...  
Keyword(s):  
T Cells ◽  
B Cells ◽  
Cd8 T Cells ◽  
Marginal Zone ◽  
Marginal Zone B Cells

scholarly journals Light chain editing generates polyreactive antibodies in chronic graft-versus-host reaction

2006 ◽  
Vol 203 (7) ◽  
pp. 1761-1772 ◽  
Author(s):  
Esther J. Witsch ◽  
Hong Cao ◽  
Hidehiro Fukuyama ◽  
Martin Weigert
Keyword(s):  
T Cells ◽  
B Cells ◽  
Transgenic Mice ◽  
Marginal Zone ◽  
Basic Protein ◽  
Autoimmune Response ◽  
Graft Versus Host Reaction ◽  
Host Reaction ◽  
Graft Versus Host ◽  
Polyreactive Antibodies

The chronic graft-versus-host (cGvH) reaction is a model of induced lupus caused by alloreactive CD4+ T cells from a Bm-12 mouse in a C57BL/6 recipient. We used this cGvH reaction in C57BL/6 anti-DNA H chain transgenic mice, 56R/B6, to understand the structure, specificity, and origin of the induced autoantibodies (auto-Abs). We found anti-DNA Abs that reacted to several different antigens, such as phosphatidylserine, myelin basic protein, thyroglobulin, histone, insulin, cytochrome C, and β-galactosidase. This polyreactivity was found for Abs from B cells that expressed the 56R H chain transgene with “editor” L chains that did not completely veto autoreactivity. We suggest that such incomplete editing results in polyreactivity and that incompletely edited polyreactive B cells influence the subsequent expression of pathogenic auto-Abs in disease. We also found B cells that coexpress κ and λ L chain. These B cells contributed to the autoimmune response and are possibly in the marginal zone of the spleen.

scholarly journals Peripheral blood lymphocyte receptors for B-lymphoblastoid cell lines (B-LCL)

Blood ◽  
1980 ◽  
Vol 56 (4) ◽  
pp. 690-695
Author(s):  
J Zighelboim ◽  
A Lichtenstein
Keyword(s):  
Immune Response ◽  
T Cells ◽  
B Cells ◽  
T Lymphocytes ◽  
Cell Lines ◽  
Peripheral Blood ◽  
Human Peripheral Blood ◽  
Wide Distribution ◽  
Lymphoblastoid Cell Lines ◽  
Surface Receptor

Because interactions between B cells and T lymphoyctes are of fundamental importance in the generation of the immune response to most antigens, we attempted to identify the cells capable of binding B- lymphoblastoid cell lines (B-LCL), their tissue distribution, and their presence in other species. Cells bearing a surface receptor for B-LCL were found in human peripheral blood, tonsil, and bone marrow, as well as mouse and rat spleen. Binding cells were phenotypically heterogeneous. The majority are T cells as defined by their ability to bind sheep red blood cells (E-rosettes). However, a subpopulation of non-T-lymphocytes were capable of binding B-LCL. This was demonstrated by depleting T cells with an E-rosette centrifugation technique and then performing a double rosette assay. The wide distribution of T lymphocytes with receptors for B-lymphoblastoid cells within peripheral lymphoid organs and their presence in several species suggest that these surface molecules may represent one of the means by which T cells and B cells interact in the induction of the immune response to T- dependent antigens.

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