Specific T-cell-mediated killing of autologous lung tumour cells

1980 ◽  
Vol 55 (1) ◽  
pp. 12-19 ◽  
Author(s):  
B.M. Vose
Keyword(s):  
T Cell ◽  
2007 ◽  
Vol 25 (18_suppl) ◽  
pp. 18513-18513
Author(s):  
D. Morales ◽  
B. E. Beltran ◽  
C. Castañeda ◽  
A. Carrasco ◽  
P. Quiñones ◽  
...  

18513 Background: Foxp3 is a key regulatory gene required for the development and function of: regulatory CD4+CD25high T cells (Treg) specialized in maintaining the balance between immunity and tolerance and activated conventional CD4+CD25low T cells without suppressive activity. Previous studies had reported the origin of Adult T-cell Leukemia/Lymphoma cells (ATLL) in Foxp3 T cells and in other lymphomas types the FOXP3 expression was only detected in the reactive T-cell background. Our objetive was to determine the presence of Treg phenotype cells by the FOXP3 expression in T-cell lymphomas. Methods: A retrospective study was performed on 48 samples collected from diverse T-cell lymphomas in our institution. A highly sensitive immunohistochemical method was used to demonstrate Treg phenotype by FOXP3 protein expression with a mouse monoclonal antibody (clone 236A/E7ABCAM) in most formalin-fixed paraffin-embedded tissue sections from lymph nodes, skin, bone marrow and extranodal sites samples as cavum and stomach. We did not co-stained with CD25 and considered a FOXP3+ tissue when positivity was > 20% of tumor cells. The statistical method was descriptive and survival was calculated using the Kaplan-Meier method. Results: Among the 48 evaluable T-cell lymphomas collected, 33 were ATLL, 8 unspecified peripheral T-cell lymphomas (U-PTCL), 6 mycosis fungoides (MF) and 1 cutaneous aggressive epidermotropic CD8(+) cytotoxic T-cell lymphoma. Among the 33 ATLL: lymphomatous=17, acute=11, smoldering=1, chronic=1, cutaneous=1 and undefined=2. FOXP3 expression in tumour cells was detected in 24% (8/33) of ATLL cases and in 37% (3/8) of U-PTCL. It was negative in MF tumour cells and aggressive epidermotropic CD8(+) cytotoxic T-cell lymphoma Among the ATLL cases FOXP3 positivity were obtained in 35% (6/17) of lymphomatous type; 18% (2/11) of acute ones and none in others ATLL types studied. Interestingly 3 U-PTCL had Treg phenotype and were related to EBV (LMP1 positive); two had extranodal primary ( parotide and cavum) and one was nodal. We failed to demonstrate any correlation between FOXP3 status and survival. Conclusions: Some ATLL and U-PTCL had Treg phenotype. In our work Foxp3 expression was not found to be a prognostic factor. No significant financial relationships to disclose.


2016 ◽  
Vol 61 ◽  
pp. S218
Author(s):  
J. Wahba ◽  
M. Natoli ◽  
L. Whilding ◽  
A. Parente-Pereira ◽  
J. Maher ◽  
...  

Leukemia ◽  
2003 ◽  
Vol 17 (5) ◽  
pp. 894-899 ◽  
Author(s):  
P Kokhaei ◽  
M R Rezvany ◽  
L Virving ◽  
A Choudhury ◽  
H Rabbani ◽  
...  

2018 ◽  
Vol 420 ◽  
pp. 146-155 ◽  
Author(s):  
Marie Guerard ◽  
Thomas Robin ◽  
Pascal Perron ◽  
Anne-Sophie Hatat ◽  
Laurence David-Boudet ◽  
...  

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Zhaojuan Yang ◽  
Guiqin Xu ◽  
Boshi Wang ◽  
Yun Liu ◽  
Li Zhang ◽  
...  

AbstractOncogenic activation of KRAS and its surrogates is essential for tumour cell proliferation and survival, as well as for the development of protumourigenic microenvironments. Here, we show that the deubiquitinase USP12 is commonly downregulated in the KrasG12D-driven mouse lung tumour and human non-small cell lung cancer owing to the activation of AKT-mTOR signalling. Downregulation of USP12 promotes lung tumour growth and fosters an immunosuppressive microenvironment with increased macrophage recruitment, hypervascularization, and reduced T cell activation. Mechanistically, USP12 downregulation creates a tumour-promoting secretome resulting from insufficient PPM1B deubiquitination that causes NF-κB hyperactivation in tumour cells. Furthermore, USP12 inhibition desensitizes mouse lung tumour cells to anti-PD-1 immunotherapy. Thus, our findings propose a critical component downstream of the oncogenic signalling pathways in the modulation of tumour-immune cell interactions and tumour response to immune checkpoint blockade therapy.


Immunobiology ◽  
2012 ◽  
Vol 217 (7) ◽  
pp. 719-729 ◽  
Author(s):  
Yehia S. Mohamed ◽  
Debbie Dunnion ◽  
Iryna Teobald ◽  
Renata Walewska ◽  
Michael J. Browning

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