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Anti-Syk Antibody, Unconjugated


Antibody ID


Target Antigen

Syk human, mouse

Proper Citation

(Cell Signaling Technology Cat# 2712, RRID:AB_2197223)




Applications: W. Consolidation on 11/2018: AB_10691458, AB_10828107, AB_2197223.


Cell Signaling Technology

Cat Num


Publications that use this research resource

Loss of the HVEM Tumor Suppressor in Lymphoma and Restoration by Modified CAR-T Cells.

  • Boice M
  • Cell
  • 2016 Oct 6

Literature context:


The HVEM (TNFRSF14) receptor gene is among the most frequently mutated genes in germinal center lymphomas. We report that loss of HVEM leads to cell-autonomous activation of B cell proliferation and drives the development of GC lymphomas in vivo. HVEM-deficient lymphoma B cells also induce a tumor-supportive microenvironment marked by exacerbated lymphoid stroma activation and increased recruitment of T follicular helper (TFH) cells. These changes result from the disruption of inhibitory cell-cell interactions between the HVEM and BTLA (B and T lymphocyte attenuator) receptors. Accordingly, administration of the HVEM ectodomain protein (solHVEM(P37-V202)) binds BTLA and restores tumor suppression. To deliver solHVEM to lymphomas in vivo, we engineered CD19-targeted chimeric antigen receptor (CAR) T cells that produce solHVEM locally and continuously. These modified CAR-T cells show enhanced therapeutic activity against xenografted lymphomas. Hence, the HVEM-BTLA axis opposes lymphoma development, and our study illustrates the use of CAR-T cells as "micro-pharmacies" able to deliver an anti-cancer protein.

Funding information:
  • NIMH NIH HHS - T32 MH019983(United States)