scholarly journals T and B Cells in Periodontal Disease: New Functions in A Complex Scenario

2019 ◽  
Vol 20 (16) ◽  
pp. 3949 ◽  
Author(s):  
C.M. Figueredo ◽  
R. Lira-Junior ◽  
R.M. Love
Keyword(s):  
T Cells ◽  
B Cells ◽  
Bone Loss ◽  
Periodontal Disease ◽  
B Cell ◽  
Dependent Manner ◽  
T And B Cells ◽  
Activated T Cells ◽  
Mait Cells

Periodontal disease is characterised by a dense inflammatory infiltrate in the connective tissue. When the resolution is not achieved, the activation of T and B cells is crucial in controlling chronic inflammation through constitutive cytokine secretion and modulation of osteoclastogenesis. The present narrative review aims to overview the recent findings of the importance of T and B cell subsets, as well as their cytokine expression, in the pathogenesis of the periodontal disease. T regulatory (Treg), CD8+ T, and tissue-resident γδ T cells are important to the maintenance of gingival homeostasis. In inflamed gingiva, however, the secretion of IL-17 and secreted osteoclastogenic factor of activated T cells (SOFAT) by activated T cells is crucial to induce osteoclastogenesis via RANKL activation. Moreover, the capacity of mucosal-associated invariant T cells (MAIT cells) to produce cytokines, such as IFN-γ, TNF-α, and IL-17, might indicate a critical role of such cells in the disease pathogenesis. Regarding B cells, low levels of memory B cells in clinically healthy periodontium seem to be important to avoid bone loss due to the subclinical inflammation that occurs. On the other hand, they can exacerbate alveolar bone loss in a receptor activator of nuclear factor kappa-B ligand (RANKL)-dependent manner and affect the severity of periodontitis. In conclusion, several new functions have been discovered and added to the complex knowledge about T and B cells, such as possible new functions for Tregs, the role of SOFAT, and MAIT cells, as well as B cells activating RANKL. The activation of distinct T and B cell subtypes is decisive in defining whether the inflammatory lesion will stabilise as chronic gingivitis or will progress to a tissue destructive periodontitis.

Antibody Production Remains Intact Despite Loss of Bone Marrow B cells in Murine Norovirus Infected Stat1−/− Mice

2021 ◽  
Author(s):  
Daniel E Eldridge ◽  
Charlie C Hsu
Keyword(s):  
Bone Marrow ◽  
B Cells ◽  
B Cell ◽  
Cell Loss ◽  
Dependent Manner ◽  
Intestinal Epithelial ◽  
Murine Norovirus ◽  
Laboratory Mice ◽  
T And B Cells ◽  
Humoral Immune

Murine norovirus (MNV), which can be used as a model system to study human noroviruses, can infect macrophages/monocytes, neutrophils, dendritic, intestinal epithelial, T and B cells, and is highly prevalent in laboratory mice. We previouslyshowed that MNV infection significantly reduces bone marrow B cell populations in a Stat1-dependent manner. We show here that while MNV-infected Stat1−/− mice have significant losses of bone marrow B cells, splenic B cells capable of mounting an antibody response to novel antigens retain the ability to expand. We also investigated whether increased granulopoiesis after MNV infection was causing B cell loss. We found that administration of anti-G-CSF antibody inhibits the pronounced bone marrow granulopoiesis induced by MNV infection of Stat1−/− mice, but this inhibition did not rescue bone marrow B cell losses. Therefore, MNV-infected Stat1−/− mice can still mount a robust humoral immune response despite decreased bone marrow B cells. This suggests that further investigation will be needed to identify other indirect factors or mechanisms that are responsible for the bone marrow B cell losses seen after MNV infection. In addition, this work contributes to our understanding of the potential physiologic effects of Stat1-related disruptions in research mouse colonies that may be endemically infected with MNV.

scholarly journals Effect of Human Mesenchymal Stem Cells on Xenogeneic T and B Cells Isolated from Lupus-Prone MRL.Faslpr Mice

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Hong Kyung Lee ◽  
Eun Young Kim ◽  
Hyung Sook Kim ◽  
Eun Jae Park ◽  
Hye Jin Lee ◽  
...  
Keyword(s):  
Stem Cells ◽  
T Cells ◽  
Mesenchymal Stem Cells ◽  
B Cells ◽  
Lupus Erythematosus ◽  
Human Mesenchymal Stem Cells ◽  
Preclinical Studies ◽  
Dependent Manner ◽  
T And B Cells

Systemic lupus erythematosus (SLE) is an autoimmune disease, which is characterized by hyperactivation of T and B cells. Human mesenchymal stem cells (hMSCs) ameliorate the progression of SLE in preclinical studies using lupus-prone MRL.Faslpr mice. However, whether hMSCs inhibit the functions of xenogeneic mouse T and B cells is not clear. To address this issue, we examined the in vitro effects of hMSCs on T and B cells isolated from MRL.Faslpr mice. Naïve hMSCs inhibited the functions of T cells but not B cells. hMSCs preconditioned with IFN-γ (i) inhibited the proliferation of and IgM production by B cells, (ii) attracted B cells for cell–cell interactions in a CXCL10-dependent manner, and (iii) inhibited B cells by producing indoleamine 2,3-dioxygenase. In summary, our data demonstrate that hMSCs exert therapeutic activity in mice in three steps: first, naïve hMSCs inhibit the functions of T cells, hMSCs are then activated by IFN-γ, and finally, they inhibit B cells.

scholarly journals Activated CD4+CD25+ T cells selectively kill B lymphocytes

Blood ◽  
2006 ◽  
Vol 107 (10) ◽  
pp. 3925-3932 ◽  
Author(s):  
Dong-Mei Zhao ◽  
Angela M. Thornton ◽  
Richard J. DiPaolo ◽  
Ethan M. Shevach
Keyword(s):  
Cell Proliferation ◽  
T Cells ◽  
Cell Death ◽  
B Cells ◽  
B Cell ◽  
T Cell Activation ◽  
Fas Ligand ◽  
Cell Function ◽  
Cell Contact ◽  
Dependent Manner

The suppressive capacity of naturally occurring mouse CD4+CD25+ T cells on T-cell activation has been well documented. The present study is focused on the interaction of CD4+CD25+ T cells and B cells. By coculturing preactivated CD4+CD25+ T cells with B cells in the presence of polyclonal B-cell activators, we found that B-cell proliferation was significantly suppressed. The suppression of B-cell proliferation was due to increased cell death caused by the CD4+CD25+ T cells in a cell-contact–dependent manner. The induction of B-cell death is not mediated by Fas–Fas ligand pathway, but surprisingly, depends on the up-regulation of perforin and granzymes in the CD4+CD25+ T cells. Furthermore, activated CD4+CD25+ T cells preferentially killed antigen-presenting but not bystander B cells. Our results demonstrate that CD4+CD25+ T cells can act directly on B cells and suggest that the prevention of autoimmunity by CD4+CD25+ T cells can be explained, at least in part, by the direct regulation of B-cell function.

scholarly journals In VitroMeasles Virus Infection of Human Lymphocyte Subsets Demonstrates High Susceptibility and Permissiveness of both Naive and Memory B Cells

2018 ◽  
Vol 92 (8) ◽  
pp. e00131-18 ◽  
Author(s):  
Brigitta M. Laksono ◽  
Christina Grosserichter-Wagener ◽  
Rory D. de Vries ◽  
Simone A. G. Langeveld ◽  
Maarten D. Brem ◽  
...  
Keyword(s):  
T Cells ◽  
B Cells ◽  
B Cell ◽  
Immune Suppression ◽  
Peripheral Blood ◽  
Measles Virus ◽  
Memory B Cells ◽  
T And B Cells ◽  
B Cell Subsets

ABSTRACTMeasles is characterized by a transient immune suppression, leading to an increased risk of opportunistic infections. Measles virus (MV) infection of immune cells is mediated by the cellular receptor CD150, expressed by subsets of lymphocytes, dendritic cells, macrophages, and thymocytes. Previous studies showed that human and nonhuman primate memory T cells express higher levels of CD150 than naive cells and are more susceptible to MV infection. However, limited information is available about the CD150 expression and relative susceptibility to MV infection of B-cell subsets. In this study, we assessed the susceptibility and permissiveness of naive and memory T- and B-cell subsets from human peripheral blood or tonsils toin vitroMV infection. Our study demonstrates that naive and memory B cells express CD150, but at lower frequencies than memory T cells. Nevertheless, both naive and memory B cells proved to be highly permissive to MV infection. Furthermore, we assessed the susceptibility and permissiveness of various functionally distinct T and B cells, such as helper T (TH) cell subsets and IgG- and IgA-positive memory B cells, in peripheral blood and tonsils. We demonstrated that TH1TH17 cells and plasma and germinal center B cells were the subsets most susceptible and permissive to MV infection. Our study suggests that both naive and memory B cells, along with several other antigen-experienced lymphocytes, are important target cells of MV infection. Depletion of these cells potentially contributes to the pathogenesis of measles immune suppression.IMPORTANCEMeasles is associated with immune suppression and is often complicated by bacterial pneumonia, otitis media, or gastroenteritis. Measles virus infects antigen-presenting cells and T and B cells, and depletion of these cells may contribute to lymphopenia and immune suppression. Measles has been associated with follicular exhaustion in lymphoid tissues in humans and nonhuman primates, emphasizing the importance of MV infection of B cellsin vivo. However, information on the relative susceptibility of B-cell subsets is scarce. Here, we compared the susceptibility and permissiveness toin vitroMV infection of human naive and memory T- and B-cell subsets isolated from peripheral blood or tonsils. Our results demonstrate that both naive and memory B cells are more permissive to MV infection than T cells. The highest infection levels were detected in plasma cells and germinal center B cells, suggesting that infection and depletion of these populations contribute to reduced host resistance.

scholarly journals Production and characterization of a bispecific IgG capable of inducing T-cell-mediated lysis of malignant B cells

Blood ◽  
1993 ◽  
Vol 81 (12) ◽  
pp. 3343-3349 ◽  
Author(s):  
BK Link ◽  
GJ Weiner
Keyword(s):  
T Cells ◽  
T Cell ◽  
B Cells ◽  
B Cell ◽  
Hybridoma Cells ◽  
Activated T Cells ◽  
Human B Cells ◽  
B Cell Malignancy ◽  
Cell Malignancy

Abstract Bispecific monoclonal antibodies (bsabs) recognizing both CD3 and a tumor antigen can redirect T-cell-mediated cytotoxicity toward cells bearing that antigen. Such bsabs have been shown to be more effective than monospecific monoclonal antibodies (MoAbs) at preventing tumor growth in animal models of B-cell malignancy. The current studies describe the production and preliminary evaluation of a bsab designed to induce the lysis of malignant human B cells by human T cells. The bsab was obtained from a hybrid-hybridoma cell line produced by fusing OKT3-secreting hybridoma cells with hybridoma cells that secrete 1D10. 1D10 is an MoAb that recognizes an antigen found on a majority of malignant human B cells that has not been detected to a significant degree on normal resting or activated lymphocytes. High performance liquid chromatography (HPLC) was used to separate bsab from monospecific antibodies that were also present in the hybrid-hybridoma antibody product. The bsab was then evaluated in vitro for its ability to induce lysis of malignant B cells by activated T cells. The bsab consistently induced extensive lysis in vitro of 1D10 (+) cells, including both cell lines and cells obtained from patients with a variety of B-cell malignancies. No such effect was seen with activated T cells alone or activated T cells with monospecific antibody. No increased lysis was seen with 1D10 (-) cell lines. The bsab also mediated lysis of malignant B cells by autologous T cells. We conclude bsab containing an OKT3 arm and a 1D10 arm can induce T-cell-mediated lysis in a manner that is both potent and specific. This supports further evaluation of this bsab as a potential immunotherapy of B-cell malignancy.

scholarly journals The allogeneic bisection of carrier-specific enhancement of monoclonal B-cell responses.

1975 ◽  
Vol 142 (5) ◽  
pp. 1165-1179 ◽  
Author(s):  
S K Pierce ◽  
N R Klinman
Keyword(s):  
T Cells ◽  
B Cells ◽  
B Cell ◽  
Immunoglobulin Class ◽  
Cell Responses ◽  
Cell Clones ◽  
Ia Antigens ◽  
Collaborative Interactions ◽  
B Cell Responses

The ability of T cells to enhance the response of syngeneic and allogeneic B cells to thymus-dependent hapten-carrier conjugates was analyzed. This analysis was carried out on individual primary B cells in splenic fragment cultures derived from irradiated reconstituted mice. This system has several advantages: (a) the response of the B cells is entirely dependent on carrier priming of the irradiated recipient; (b) this B-cell response can be quantitated in terms of the number of responding cells; and (c) very small B-cell responses can be readily detected and analyzed. The results indicate that the majority of hapten-specific B cells were stimulated in allogeneic and syngeneic recipients only if these recipients were previously carrier primed. The number of B cells responding in carrier-primed allogeneic recipients was 60-70% of that in syngeneic carrier-primed recipients. The antibody-forming cell clones resulting from B cells stimulated in the allogeneic environment produced small amounts of antibody and antibody solely of the IgM immunoglobulin class, while the larger responses in syngeneic recipients were predominantly IgG1 or IgM plus IgG1. The capacity of collaborative interactions between carrier-primed T cells and primary B cells to yield IgG1 antibody-producing clones was shown to be dependent on syngeny between these cells in the H-2 gene complex. It is concluded that: (a) B cells can be triggered by T-dependent antigens to clone formation through collaboration with T cells which differ at the H-2 complex as long as these T cells recognize the antigen; (b) the immunoglobulin class produced by the progeny of stimulated B cells generally depends on the nature of the stimulatory event rather than the nature of the B cell itself; and (c) stimulation to IgG1 production is dependent on syngeny between the collaborating T and B cells probably within the Ir-1A region. The role of the Ia antigens in the formation of IgG1-producing clones is not yet clear; Ia identity could permit IgG1 production or, conversely, nonidentity of Ia could induce all allogeneic interactions which prohibit IgG1 production.

scholarly journals Selective inhibition of growth factor-dependent human B cell proliferation by monoclonal antibody AB1 to an antigen expressed by activated B cells.

1984 ◽  
Vol 160 (6) ◽  
pp. 1919-1924 ◽  
Author(s):  
L K Jung ◽  
S M Fu
Keyword(s):  
Monoclonal Antibody ◽  
Cell Proliferation ◽  
T Cells ◽  
B Cells ◽  
B Cell ◽  
Leukemic Cells ◽  
Activated T Cells ◽  
Igm Antibodies ◽  
Stimulatory Factor ◽  
Activated B Cells

A monoclonal antibody, AB1, was established with activated human B cells as immunogen. AB1 stained activated B cells but not activated T cells. Its selective reactivity to activated B cells was further documented by its nonreactivity to activated T cells, resting T and B cells, monocytes, granulocytes, bone marrow cells, leukemic cells, and cells from cell lines of T, B, and myeloid lineages. Upon activation, the antigen appeared on B cells as early as 3-4 h after stimulation and was fully expressed by 38 h. The expression of this antigen was not dependent on the presence of B cell stimulatory factor(s). Anti-IgM antibodies by themselves induced its expression. AB1 inhibited B cell proliferation that was induced by a low dose anti-IgM antibody and conditioned medium containing B cell stimulatory factor. It did not inhibit B cell proliferation induced by either high doses of anti-IgM antibodies or by formalinized Staphylococcus aureus. It also failed to inhibit T cell mitogenesis. The possibility exists that this antigen is related to the receptor for B cell stimulatory factor.

scholarly journals Interaction of B cells with activated T cells reduces the threshold for CD40-mediated B cell activation

1999 ◽  
Vol 11 (1) ◽  
pp. 71-79 ◽  
Author(s):  
Gerry G. B. Klaus ◽  
Mary Holman ◽  
Caroline Johnson-Léger ◽  
Jillian R. Christenson ◽  
Marilyn R. Kehry
Keyword(s):  
T Cells ◽  
B Cells ◽  
B Cell ◽  
Cell Activation ◽  
B Cell Activation ◽  
Activated T Cells

RhoF GTPase Transcription Is Upregulated in Germinal Center B-Cells, Shows Altered Expression in Malignant B-Cells, and Interacts with the ATM Pathway.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 285-285
Author(s):  
Launce G. Gouw ◽  
N. Scott Reading ◽  
David K. Crockett ◽  
Philippe Szankasi ◽  
Megan S. Lim ◽  
...  
Keyword(s):  
T Cells ◽  
B Cells ◽  
B Cell ◽  
Germinal Center ◽  
De Novo ◽  
Cell Lymphoma ◽  
Lymphocyte Subpopulations ◽  
Interacting Proteins ◽  
Tissue Samples

Abstract Follicular lymphoma (FL) is the most common low-grade B-cell non Hodgkin lymphoma in the Western hemisphere. A significant proportion of FL undergo histologic transformation to diffuse large B-cell lymphoma (DLBCL). Using cDNA microarray analysis, we identified an expressed sequence tag GI#10952525 consistently differentially expressed in transformed follicular lymphomas (tFL). This was characterized as RhoF, a novel member of the Rho family. Rho GTPases play central roles in cytoskeletal dynamics, cell-cell interactions, and intracellular signaling pathways involved in migration, proliferation and survival. Dysregulation of Rho proteins are key events implicated in tumorigenesis. To define the role of RhoF in lymphocyte physiology and lymphoma transformation, we assessed its expression across phenotypically defined lymphocyte subpopulations, using quantitative real-time PCR. We determined relative RhoF levels in immunomagnetic bead purified normal lymphoid subpopulations [naïve B-cells, memory B-cells, germinal center B-cells and T-cells], reactive lymphoid tissues (n=5), cell lines [derived from t(14;18) tFL (n =3), de novo DLBCL (n=7), and T-cell malignancy (n=3)] and tissue from primary human lymphoid neoplasms [FL (n=5), de novo DLBCL (n=5), tFL (n=5), CLL/SLL (n=4), anaplastic large cell lymphoma (n=8), mantle cell lymphoma (n=5), and T-cell acute lymphoblastic leukemia (n=5)]. RhoF was expressed at significantly higher levels in B-cells relative to T-cells. We saw this pattern in purified lymphocyte subpopulations, in cell lines, and in primary lymphoma tissue samples. Notably, we detected elevated levels of RhoF transcript in B-cells of germinal center (GC) origin, both in the reactive and neoplastic samples of GC-derived B-cells. The highest transcriptional levels of RhoF were in malignant B-cells of GC origin; both in heterogeneous primary tissue samples and in homogeneous tissue culture preparations. To investigate its functional role, we cloned RhoF into a vector coding for a C-terminal polyhistidine- and V5 epitope-tag. We expressed the constructs in HEK 293T cells, and purified the RhoF-containing complexes using a tandem affinity purification approach. We ran cell lysates through a nickel column; non-interacting proteins were washed off under native conditions and the bound RhoF complexes eluted with imidazole. Eluate was immunoprecipitated with sepharose-bound anti-V5 antibody. Immunoprecipitated complexes were denatured and resolved by 1D-PAGE. Unique bands representing RhoF interacting proteins were isolated and enzymatically cleaved with trypsin. Resultant peptides underwent liquid chromatography and tandem mass spectrometry. Data were searched against the NCBI nr.FASTA nonredundant protein database using the SEQUEST algorithm and false positive rates determined with INTERACT and ProteinProphet. Among several putative RhoF interactors, we identified ATM as an important RhoF binding partner. In conclusion, our demonstration of the differential expression of RhoF in GC-derived cells and its upregulation in tFL provide evidence for a connection between the role of this novel protein in B-cell development and malignancy. In addition, evidence of an association between RhoF and ATM may provide a link between DNA repair, cell cycle control and morphological dynamics.

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