scholarly journals Diminished bone regeneration after debridement of posttraumatic osteomyelitis is accompanied by altered cytokine levels, elevated B cell activity, and increased osteoclast activity

2017 ◽  
Vol 35 (11) ◽  
pp. 2425-2434 ◽  
Author(s):  
Johannes M. Wagner ◽  
Henriette Jaurich ◽  
Christoph Wallner ◽  
Stephanie Abraham ◽  
Mustafa Becerikli ◽  
...  
Keyword(s):  
B Cell ◽  
Bone Regeneration ◽  
Cell Activity ◽  
Posttraumatic Osteomyelitis ◽  
Osteoclast Activity ◽  
Cytokine Levels

Regulators of B-cell activity in SLE: a better target for treatment than B-cell depletion?

Lupus ◽  
2009 ◽  
Vol 18 (7) ◽  
pp. 575-580 ◽  
Author(s):  
S Dolff ◽  
WH Abdulahad ◽  
M Bijl ◽  
CGM Kallenberg
Keyword(s):  
B Cell ◽  
Cell Activity ◽  
Cell Depletion ◽  
B Cell Depletion

Hepatocyte growth factor enhances B-cell activity

Life Sciences ◽  
1993 ◽  
Vol 53 (5) ◽  
pp. PL89-PL93 ◽  
Author(s):  
Bryan Delaney ◽  
Woo S. Koh ◽  
Kyu H. Yang ◽  
Stephen C. Strom ◽  
Norbert F. Kaminski
Keyword(s):  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
B Cell ◽  
Cell Activity ◽  
Hepatocyte Growth

scholarly journals Defective T cell-mediated, isotype-specific immunoglobulin regulation in B cell chronic lymphocytic leukemia

Blood ◽  
1988 ◽  
Vol 71 (4) ◽  
pp. 1012-1020 ◽  
Author(s):  
JS Moore ◽  
MB Prystowsky ◽  
RG Hoover ◽  
EC Besa ◽  
PC Nowell
Keyword(s):  
T Cells ◽  
T Cell ◽  
B Cells ◽  
Chronic Lymphocytic Leukemia ◽  
B Cell ◽  
Cell Activity ◽  
Lymphocytic Leukemia ◽  
Specific Immunoglobulin ◽  
Cell Chronic Lymphocytic Leukemia

The consistent occurrence of T cell abnormalities in patients with B cell chronic lymphocytic leukemia (B-CLL) suggest that the non- neoplastic host T cells may be involved in the pathogenesis of this B cell neoplasm. Because potential defects of immunoglobulin regulation are evident in B-CLL patients, we investigated one aspect of this by studying the T cell-mediated immunoglobulin isotype-specific immunoregulatory circuit in B-CLL. The existence of class-specific immunoglobulin regulatory mechanisms mediated by Fc receptor-bearing T cells (FcR + T) through soluble immunoglobulin binding factors (IgBFs) has been well established in many experimental systems. IgBFs can both suppress and enhance B cell activity in an isotype-specific manner. We investigated the apparently abnormal IgA regulation in a B-CLL patient (CLL249) whose B cells secrete primarily IgA in vitro. Enumeration of FcR + T cells showed a disproportionate increase in IgA FcR + T cells in the peripheral blood of this patient. Our studies showed that the neoplastic B cells were not intrinsically unresponsive to the suppressing component of IgABF produced from normal T cells, but rather the IgABF produced by the CLL249 host T cells was defective. CLL249 IgABF was unable to suppress IgA secretion by host or normal B cells and enhanced the in vitro proliferation of the host B cells. Size fractionation of both normal and CLL249 IgABF by gel-filtration high- performance liquid chromatography (HPLC) demonstrated differences in the ultraviolet-absorbing components of IgABF obtained from normal T cells v that from our patient with defective IgA regulation. Such T cell dysfunction may not be restricted to IgA regulation, since we have found similar expansion of isotype-specific FcR + T cells associated with expansion of the corresponding B cell clone in other patients with B-CLL. These data suggest that this T cell-mediated regulatory circuit could be significantly involved in the pathogenesis of B-CLL.

scholarly journals Hemolysis Inhibits Humoral B Cell Responses and Modulates Alloimmunization Risk in Patients with Sickle Cell Disease

Blood ◽  
2020 ◽  
Author(s):  
Mouli Pal ◽  
Weili Bao ◽  
Rikang Wang ◽  
Yunfeng Liu ◽  
Xiuli An ◽  
...  
Keyword(s):  
B Cells ◽  
Sickle Cell Disease ◽  
B Cell ◽  
Sickle Cell ◽  
Cell Response ◽  
Cell Activity ◽  
Immunomodulatory Activity ◽  
Heme Oxygenase 1 ◽  
Cell Disease ◽  
B Cell Response

Red blood cell alloimmunization remains a barrier for safe and effective transfusions in sickle cell disease (SCD), but the associated risk factors remain largely unknown. Intravascular hemolysis, a hallmark of SCD, results in the release of heme with potent immunomodulatory activity, although its effect on SCD humoral response, specifically alloimmunization, remains unclear. Here, we found that cell-free heme suppresses human B cell plasmablast/plasma cell differentiation by inhibiting the DOCK8/STAT3 signaling pathway, which is critical for B cell activation, as well as by upregulating heme oxygenase 1 (HO-1) through its enzymatic byproducts, carbon monoxide and biliverdin. Whereas non-alloimmunized SCD B cells were inhibited by exogenous heme, B cells from the alloimmunized group were non-responsive to heme inhibition and readily differentiated into plasma cells. Consistent with a differential B cell response to hemolysis, we found elevated B cell basal levels of DOCK8 and higher HO-1-mediated inhibition of activated B cells in non-alloimmunized compared to alloimmunized SCD patients. To overcome the alloimmunized B cell heme insensitivity, we screened several heme-binding molecules and identified quinine as a potent inhibitor of B cell activity, reversing the resistance to heme suppression in alloimmunized patients. B cell inhibition by quinine only occurred in the presence of heme and through HO-1 induction. Altogether, these data suggest that hemolysis can dampen the humoral B cell response and that B cell heme responsiveness maybe a determinant of alloimmunization risk in SCD. Quinine by restoring B cell heme sensitivity may have therapeutic potential to prevent and inhibit alloimmunization in SCD patients.

scholarly journals Omics-wide quantitative B-cell infiltration analyses identify GPR18 for human cancer prognosis with superiority over CD20

2020 ◽  
Vol 3 (1) ◽  
Author(s):  
Yuchen Liu ◽  
Li Wang ◽  
Kwok-Wai Lo ◽  
Vivian Wai Yan Lui
Keyword(s):  
T Cell ◽  
B Cell ◽  
B Lymphocyte ◽  
Human Cancer ◽  
Single Gene ◽  
Cell Activity ◽  
Cancer Prognosis ◽  
Low Grade ◽  
Functional Link ◽  
Human Cancers

AbstractTumor-infiltrating B lymphocyte (TIL-B), and TIL-B-related biomarkers have clinical prognostic values for human cancers. CD20 (encoded by MS4A1) is a widely used TIL-B biomarker. Using TCGA-quantitative multiomics datasets, we first cross-compare prognostic powers of intratumoral CD20 protein, mRNA and TIL-B levels in pan-cancers. Here, we show that MS4A1 and TIL-B are consistently prognostic in 5 cancers (head and neck, lung, cervical, kidney and low-grade glioma), while unexpectedly, CD20 protein levels lack quantitative correlations with MS4A1/TIL-B levels and demonstrate limited prognosticity. Subsequent bioinformatics discovery for TIL-B prognostic gene identifies a single gene, GPR18 with stand-alone prognosticity across 9 cancers (superior over CD20), with further validations in multiple non-TCGA cohorts. GPR18's immune signature denotes major B-cell-T-cell interactions, with its intratumoral expression strongly tied to a “T-cell active”, likely cytolytic, status across human cancers, suggesting its functional link to cytolytic T-cell activity in cancer. GPR18 merits biological and clinical utility assessments over CD20.

scholarly journals Liver fibrosis occurs through dysregulation of MyD88-dependent innate B-cell activity

Hepatology ◽  
2015 ◽  
Vol 61 (6) ◽  
pp. 2067-2079 ◽  
Author(s):  
Manoj Thapa ◽  
Raghavan Chinnadurai ◽  
Victoria M. Velazquez ◽  
Dana Tedesco ◽  
Elizabeth Elrod ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
B Cell ◽  
Cell Activity

scholarly journals Ataxin-1 regulates B cell function and the severity of autoimmune experimental encephalomyelitis

2020 ◽  
Vol 117 (38) ◽  
pp. 23742-23750 ◽  
Author(s):  
Alessandro Didonna ◽  
Ester Canto Puig ◽  
Qin Ma ◽  
Atsuko Matsunaga ◽  
Brenda Ho ◽  
...  
Keyword(s):  
B Cells ◽  
B Cell ◽  
Cell Function ◽  
Cell Activity ◽  
Cell Polarization ◽  
Spinocerebellar Ataxia Type ◽  
Loss Of Function ◽  
Th1 Cell ◽  
Aberrant Expression

Ataxin-1 (ATXN1) is a ubiquitous polyglutamine protein expressed primarily in the nucleus where it binds chromatin and functions as a transcriptional repressor. Mutant forms of ataxin-1 containing expanded glutamine stretches cause the movement disorder spinocerebellar ataxia type 1 (SCA1) through a toxic gain-of-function mechanism in the cerebellum. Conversely, ATXN1 loss-of-function is implicated in cancer development and Alzheimer’s disease (AD) pathogenesis.ATXN1was recently nominated as a susceptibility locus for multiple sclerosis (MS). Here, we show thatAtxn1-null mice develop a more severe experimental autoimmune encephalomyelitis (EAE) course compared to wildtype mice. The aggravated phenotype is mediated by increased T helper type 1 (Th1) cell polarization, which in turn results from the dysregulation of B cell activity. Ataxin-1 ablation in B cells leads to aberrant expression of key costimulatory molecules involved in proinflammatory T cell differentiation, including cluster of differentiation (CD)44 and CD80. In addition, comprehensive phosphoflow cytometry and transcriptional profiling link the exaggerated proliferation of ataxin-1 deficient B cells to the activation of extracellular signal-regulated kinase (ERK) and signal transducer and activator of transcription (STAT) pathways. Lastly, selective deletion of the physiological binding partner capicua (CIC) demonstrates the importance of ATXN1 native interactions for correct B cell functioning. Altogether, we report a immunomodulatory role for ataxin-1 and provide a functional description of theATXN1locus genetic association with MS risk.

scholarly journals Osteoclast activity modulates B-cell development in the bone marrow

Cell Research ◽  
2011 ◽  
Vol 21 (7) ◽  
pp. 1102-1115 ◽  
Author(s):  
Anna Mansour ◽  
Adrienne Anginot ◽  
Stéphane J C Mancini ◽  
Claudine Schiff ◽  
Georges F Carle ◽  
...  
Keyword(s):  
Bone Marrow ◽  
B Cell ◽  
Cell Development ◽  
B Cell Development ◽  
Osteoclast Activity

scholarly journals High frequency of normal DJH joints in B cell progenitors in severe combined immunodeficiency mice.

1993 ◽  
Vol 178 (3) ◽  
pp. 1007-1016 ◽  
Author(s):  
J L Pennycook ◽  
Y Chang ◽  
J Celler ◽  
R A Phillips ◽  
G E Wu
Keyword(s):  
Bone Marrow ◽  
B Cell ◽  
Fetal Liver ◽  
Severe Combined Immunodeficiency ◽  
Cell Activity ◽  
Scid Mice ◽  
Combined Immunodeficiency ◽  
Cell Stage ◽  
Reading Frame ◽  
B Lineage

The severe combined immunodeficiency (scid) mouse has a defective V(D)J recombinase activity that results in arrested lymphoid development at the pro-B cell stage in the B lineage. The defect is not absolute and scid mice do attempt gene rearrangement. Indeed, approximately 15% of all scid mice develop detectable levels of oligoclonal serum immunoglobulin and T cell activity. To gain more insight into the scid defect and its effect on V(D)J rearrangement, we analyzed DJH recombination in scid bone marrow. We determined that DJH structures are present in scid bone marrow and occur at a frequency only 10-100 times less than C.B-17+/+. The scid DJH repertoire is limited and resembles fetal liver DJH junctions, with few N insertions and predominant usage of reading frame 1. Moreover, 70% of the DJH structures were potentially productive, indicating that normal V(D)J recombinants should be arising continually.

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