Faculty Opinions recommendation of Human endometriosis is associated with plasma cells and overexpression of B lymphocyte stimulator.

Author(s):  
Patrick Groothuis
2007 ◽  
Vol 104 (30) ◽  
pp. 12451-12456 ◽  
Author(s):  
A. Hever ◽  
R. B. Roth ◽  
P. Hevezi ◽  
M. E. Marin ◽  
J. A. Acosta ◽  
...  

2020 ◽  
Vol 20 (18) ◽  
pp. 2316-2323 ◽  
Author(s):  
Alican Kusoglu ◽  
Bakiye G. Bagca ◽  
Neslihan P.O. Ay ◽  
Guray Saydam ◽  
Cigir B. Avci

Background: Ruxolitinib is a selective JAK1/2 inhibitor approved by the FDA for myelofibrosis in 2014 and nowadays, comprehensive investigations on the potential of the agent as a targeted therapy for haematological malignancies are on the rise. In multiple myeloma which is a cancer of plasma cells, the Interleukin- 6/JAK/STAT pathway is emerging as a therapeutic target since the overactivation of the pathway is associated with poor prognosis. Objective: In this study, our purpose was to discover the potential anticancer effects of ruxolitinib in ARH-77 multiple myeloma cell line compared to NCI-BL 2171 human healthy B lymphocyte cell line. Methods: Cytotoxic effects of ruxolitinib in ARH-77 and NCI-BL 2171 cells were determined via WST-1 assay. The autophagy mechanism induced by ruxolitinib measured by detecting autophagosome formation was investigated. Apoptotic effects of ruxolitinib were analyzed with Annexin V-FITC Detection Kit and flow cytometry. We performed RT-qPCR to demonstrate the expression changes of the genes in the IL-6/JAK/STAT pathway in ARH-77 and NCI-BL 2171 cells treated with ruxolitinib. Results: We identified the IC50 values of ruxolitinib for ARH-77 and NCI-BL 2171 as 20.03 and 33.9μM at the 72nd hour, respectively. We showed that ruxolitinib induced autophagosome accumulation by 3.45 and 1.70 folds in ARH-77 and NCI-BL 2171 cells compared to the control group, respectively. Treatment with ruxolitinib decreased the expressions of IL-6, IL-18, JAK2, TYK2, and AKT genes, which play significant roles in MM pathogenesis. Conclusion: All in all, ruxolitinib is a promising agent for the regulation of the IL-6/JAK/STAT pathway and interferes with the autophagy mechanism in MM.


2010 ◽  
Vol 37 (8) ◽  
pp. 3747-3755 ◽  
Author(s):  
Shaoli Deng ◽  
Tao Yuan ◽  
Xiaoxing Cheng ◽  
Rui Jian ◽  
Jing Jiang

2011 ◽  
Vol 650 (1) ◽  
pp. 451-457 ◽  
Author(s):  
Gang Huang ◽  
Yanchun Yang ◽  
Zhizhen Xu ◽  
Peng Zhou ◽  
Wei Gong ◽  
...  

1975 ◽  
Vol 142 (3) ◽  
pp. 549-559 ◽  
Author(s):  
R A Rudders ◽  
R Ross

An unusual B-cell proliferation was noted in an individual (Tun) which was characterized by the presence of two separate populations of chronic lymphocytic leukemia (CLL) cell staining on the surface and in the cytoplasm for either IgG(k) or IgA(k). Utilizing an idiotypic antiserum prepared from the associated serum monoclonal IgG(k) protein the idiotype was detected on the surface and in the cytoplasm of both the IgG- and IgA-bearing cell populations. These observations are consistent with a common clonal origin and a switch mechanism involving IgG and IgA synthesis. Sequential-labeling of Surface Ig and intracellular Ig with antisera conjugated to opposite fluorochromes documented the progressive maturation of the terminal differentiation of the IgA-bearing cell population at a level before morphologically distinct plasma cells. The distribution and pattern of surface and cytoplasmic IgG and IgA staining in individual cells suggest that the direction of switching is from IgG to IgA synthesis. The demonstration of shared idiotypic specificity between the IgG- and IgA-bearing populations is consistent with a transition in Ig heavy chain synthesis resulting from an alternation in the CH gene. It is concluded that certain CLL clones may manifest a switch from IgG to IgA synthesis at a level of B-cell differentiation which encompasses both the B lymphocyte and the Ig-synthesizing plasma cell.


2013 ◽  
Vol 24 (2) ◽  
pp. 141 ◽  
Author(s):  
Manuel F. Ugarte-Gil ◽  
Eduardo M. Acevedo-Vásquez ◽  
Graciela S. Alarcón

El advenimiento del uso de terapias biológicas en Reumatología ha modificado significativamente el pronóstico de pacientes portadores de artritis reumatoide (AR), artritis juvenil (AJ), espondilitis anquilosante (EA), entre otras enfermedades. A diferencia de las terapias convencionales estos productos biológicos se dirigen a los llamados blancos terapéuticos ya sea estas una línea celular, un mediador inflamatorio o un receptor de superficie. Estos compuestos son producidos por células vivas mediante la tecnología del ADN recombinante. Estos compuestos pueden tener componentes humano y animal [quiméricos (Xi), humanizados (Zu)], o completamente humanos (H) lo cual se reconoce por las letras que se incluyen en el nombre de cada uno. En el campo de la Reumatología, el primer compuesto utilizado fue el etanercept (anti-factor de necrosis tumoral o anti-TNF) aprobado en 1998, pero otros anti-TNF han demostrado su beneficio en AR, como en EA y AJ. Los inhibidores de Interleucina (IL-1) casi no se usan en AR actualmente, pero si los inhibidores de IL-6, así como los agentes contra las células B y los agonistas de CTLA-4 (Cytotoxic T lymphocyte antigen). Existe asimismo un compuesto dirigido al BLyS (B-lymphocyte stimulator) el cual se usa en lupus eritematoso sistémico y otro dirigido al receptor activador del factor nuclear κB (RANKL, receptor activator of nuclear factor-κB ligand) que se usa en osteoporosis. Con el avance en el conocimiento de la patogenia de las enfermedades reumáticas, se vienen reconociendo otra blancos terapéuticas. En los años venideros, este campo ha de expandirse en proporciones geométricas.


2020 ◽  
Author(s):  
Shahan Mamoor

Inflammatory bowel diseases (IBD) include Crohn’s Disease and Ulcerative Colitis (1). We mined published microarray data to understand how gene expression in the hematopoietic compartment of patients with Crohn’s Disease is most different from that of healthy controls (2-4). Across two datasets (2, 3), we found that BAFF, also known as the B-lymphocyte stimulator (BLyS), encoded by the gene TNFSF13B (5), was differentially expressed in the blood of patients with Crohn’s Disease . Analysis of a third dataset (4) revealed that BAFF was among the genes most differentially expressed in monocyte-derived macrophages from patients with Crohn’s Disease. Serum BAFF, fecal BAFF, and BAFF expression in the intestinal mucosa has been demonstrated to be increased in patients with IBD (6, 7). We show here that expression of BAFF in the peripheral blood of patients with Crohn’s Disease is also increased.


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