Tonsillar B Cells Do Not Express PSGL-1, but a Significant Fraction Displays the Cutaneous Lymphocyte Antigen and Exhibits Effective E- and P-Selectin Ligand Activity

2001 ◽  
Vol 126 (1) ◽  
pp. 78-90 ◽  
Author(s):  
Dieter Armerding ◽  
Robert C. Fuhlbrigge ◽  
J. David Kieffer ◽  
Thomas S. Kupper
2003 ◽  
Vol 33 (12) ◽  
pp. 3275-3283 ◽  
Author(s):  
Anu Kantele ◽  
Erkki Savilahti ◽  
Heidi Tiimonen ◽  
Katja Iikkanen ◽  
Soile Autio ◽  
...  

1999 ◽  
Vol 197 (1) ◽  
pp. 39-45 ◽  
Author(s):  
Tadashi Yoshino ◽  
Mitsuhiro Okano ◽  
Hong-Li Chen ◽  
Junjiro Tsuchiyama ◽  
Eisaku Kondo ◽  
...  

1999 ◽  
Vol 189 (2) ◽  
pp. 241-252 ◽  
Author(s):  
LiLi Tu ◽  
Martha D. Delahunty ◽  
Han Ding ◽  
Francis W. Luscinskas ◽  
Thomas F. Tedder

L-selectin mediates leukocyte rolling on vascular endothelium during inflammation. Although vascular endothelium can be activated with inflammatory cytokines to express functional L-selectin ligands, these ligands have not been well characterized. In this study, fucosyltransferase VII cDNA (Fuc-TVII) transfection of the EA.hy926 human vascular endothelial cell line (926-FtVII) induced functional L-selectin ligand expression and expression of sialyl Lewisx (sLex), as defined by HECA-452 (cutaneous lymphocyte antigen; CLA) and CSLEX-1 mAbs. Cytokine activation of human umbilical vein endothelial cells (HUVEC) also induced functional L-selectin ligand expression, with increased CLA expression and Fuc-TVII transcription. The majority of L-selectin–dependent lymphocyte attachment to activated HUVEC and 926-FtVII cells was blocked specifically by treating the endothelial cells with the HECA-452 mAb, but not the CSLEX-1 mAb. CLA-bearing ligands on vascular endothelium also required sulfation and appropriate molecular scaffolds for functional activity, but were distinct from the L-selectin ligands previously identified by the MECA-79 mAb. These findings demonstrate that the HECA-452– defined antigen, CLA, is an essential carbohydrate component of vascular L-selectin ligands.


2008 ◽  
Vol 32 (9) ◽  
pp. 1421-1426 ◽  
Author(s):  
Marshall E. Kadin ◽  
Jack L. Pinkus ◽  
Geraldine S. Pinkus ◽  
Ivan H. Duran ◽  
Christine E. Fuller ◽  
...  

2020 ◽  
Vol 20 (3) ◽  
pp. 275-282 ◽  
Author(s):  
Alvise Sernicola ◽  
Irene Russo ◽  
Micol Silic-Benussi ◽  
Vincenzo Ciminale ◽  
Mauro Alaibac

2019 ◽  
Vol 76 (22) ◽  
pp. 1825-1834
Author(s):  
Clement Chung

Abstract Purpose This article summarizes current targeted therapies that have received regulatory approval for the treatment of B- and T-cell lymphomas. Summary Over the last 20 years, new drug therapies for lymphomas of B cells and T cells have expanded considerably. Targeted therapies for B-cell lymphomas include: (1) monoclonal antibodies directed at the CD20 lymphocyte antigen, examples of which are rituximab, ofatumumab, and obinutuzumab; (2) gene transfer therapy, an example of which is chimeric antigen receptor–modified T-cell (CAR-T) therapy directed at the CD19 antigen expressed on the cell surface of both immature and mature B cells; and (3) small-molecule inhibitors (ibrutinib, acalabrutinib, copanlisib, duvelisib, and idelalisib) that target the B-cell receptor signaling pathway. Of note, brentuximab vedotin is an antibody–drug conjugate that targets CD30, another lymphocyte antigen expressed on the cell surface of both Hodgkin lymphoma (a variant of B-cell lymphoma) and some T-cell lymphomas. Although aberrant epigenetic signaling pathways are present in both B- and T-cell lymphomas, epigenetic inhibitors (examples include belinostat, vorinostat, and romidepsin) are currently approved by the Food and Drug Administration for T-cell lymphomas only. In addition, therapies that target the tumor microenvironment have been developed. Examples include mogamulizumab, bortezomib, lenalidomide, nivolumab, and pembrolizumab. In summary, the efficacy of these agents has led to the development of supportive care to mitigate adverse effects, due to the presence of on- or off-target toxicities. Conclusion The therapeutic landscape of lymphomas has continued to evolve. In turn, the efficacy of these agents has led to the development of supportive care to mitigate adverse effects, due to the presence of on- or off-target toxicities. Further opportunities are warranted to identify patients who are most likely to achieve durable response and reduce the risk of disease progression. Ongoing trials with current and investigational agents may further elucidate their place in therapy and therapeutic benefits.


2011 ◽  
Vol 187 (6) ◽  
pp. 3026-3032 ◽  
Author(s):  
Lisa M. Kelly ◽  
João P. Pereira ◽  
Tangsheng Yi ◽  
Ying Xu ◽  
Jason G. Cyster

2006 ◽  
Vol 117 (2) ◽  
pp. 418-425 ◽  
Author(s):  
Janine Bilsborough ◽  
Donald Y.M. Leung ◽  
Mark Maurer ◽  
Michael Howell ◽  
Mark Boguniewcz ◽  
...  

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