CD26 AND CD39 IN THE REGULATORY MICROENVIRONMENTS OF LYMPHOMA AFFECTED LYMPH NODES
(Abstract release date: 05/21/15)
EHA Library. DiGaetano R. 06/12/15; 102778; PB1941
Rosanna DiGaetano
Contributions
Contributions
Abstract
Abstract: PB1941
Type: Publication Only
Background
In previous reports we have described that lack of CD26 on the surface of activated CD4+T (CD38+ ) in the microenvironment of Hodgkin lymphoma (HL) suggest a T-reg immunosuppressive activity. Other studies have shown that low expression of CD26, associated with adenosine deaminase (ADA), and the presence of CD39, ectoenzyme associated with hydrolysis of extracellular ATP, might be responsible for the generation of adenosine recognized as a major mechanism of T-reg for the suppression of anti-tumor immune responses and for successful tumour escape.
Aims
Significant amount of non-clonal cells infiltrating HL is an excellent model to analyze the para-neoplastic cellular elements of the tumor microenvironment. The scope of this study was to perform lymphocyte immunophenotyping by flow cytometry (FC) from lymph node samples suspected of lymphoma with the scope of verify biomarkers of enzymatic activity favorable to the proliferation of neoplastic cells.
Methods
We have examined the relationship between the expression of CD26 and CD39 by FC on CD4+T and measured its expression on CD4 + T subset correlating to the CD26 and CD38 in 52 samples of lymph nodes (6 HL, 30 non Hodgkin lymphoma (NHL) and 16 non malignant nodes (BN).
Results
HL samples show statically differences compared to BN in the expression of CD26 (12% vs 42%; p<0,0002), CD38 (72% vs 20%; p<0,0005), CD39 (42% vs 14% ; p<0,05). When compared to NHL there is a confirmation significance in CD26 (12% vs 37%; p<0,0007), in CD38 (72% vs 25%; p<0,0009) in contrast to CD39 (42% vs 26% ; p<0,3). Among NHL cases, there were 6 relapses, that we have compared to HL: CD26 (42% vs 12; p<0,02); CD38 (23% vs 72%; p<0,04); CD39 (30% vs 42%;p<0,7).
Summary
Data confirm the activated profile (CD38+) that distinguishes HL-infiltrating cells from NHL and BN. It is more evident in HL, but in NHL microenvironment there is a tendency to a reduction of the expression of CD26 on CD4+T cells compared with BN; this, correlated with CD39 increase, might suggests an enzymatic activity with a significant adenosine accumulation in NHL too. Although the small size of the cohort, the pattern of relapsed seems similar to HL. This mimics the regulatory microenvironments that strengthens the neoplastic cells to manipulate its surrounding to avoid host immune attack suggesting a possible resistance to treatment.
Keyword(s): Cytometry, Microenvironment, Non-Hodgkin's lymphoma, T cell lymphoma
Session topic: Publication Only
Type: Publication Only
Background
In previous reports we have described that lack of CD26 on the surface of activated CD4+T (CD38+ ) in the microenvironment of Hodgkin lymphoma (HL) suggest a T-reg immunosuppressive activity. Other studies have shown that low expression of CD26, associated with adenosine deaminase (ADA), and the presence of CD39, ectoenzyme associated with hydrolysis of extracellular ATP, might be responsible for the generation of adenosine recognized as a major mechanism of T-reg for the suppression of anti-tumor immune responses and for successful tumour escape.
Aims
Significant amount of non-clonal cells infiltrating HL is an excellent model to analyze the para-neoplastic cellular elements of the tumor microenvironment. The scope of this study was to perform lymphocyte immunophenotyping by flow cytometry (FC) from lymph node samples suspected of lymphoma with the scope of verify biomarkers of enzymatic activity favorable to the proliferation of neoplastic cells.
Methods
We have examined the relationship between the expression of CD26 and CD39 by FC on CD4+T and measured its expression on CD4 + T subset correlating to the CD26 and CD38 in 52 samples of lymph nodes (6 HL, 30 non Hodgkin lymphoma (NHL) and 16 non malignant nodes (BN).
Results
HL samples show statically differences compared to BN in the expression of CD26 (12% vs 42%; p<0,0002), CD38 (72% vs 20%; p<0,0005), CD39 (42% vs 14% ; p<0,05). When compared to NHL there is a confirmation significance in CD26 (12% vs 37%; p<0,0007), in CD38 (72% vs 25%; p<0,0009) in contrast to CD39 (42% vs 26% ; p<0,3). Among NHL cases, there were 6 relapses, that we have compared to HL: CD26 (42% vs 12; p<0,02); CD38 (23% vs 72%; p<0,04); CD39 (30% vs 42%;p<0,7).
Summary
Data confirm the activated profile (CD38+) that distinguishes HL-infiltrating cells from NHL and BN. It is more evident in HL, but in NHL microenvironment there is a tendency to a reduction of the expression of CD26 on CD4+T cells compared with BN; this, correlated with CD39 increase, might suggests an enzymatic activity with a significant adenosine accumulation in NHL too. Although the small size of the cohort, the pattern of relapsed seems similar to HL. This mimics the regulatory microenvironments that strengthens the neoplastic cells to manipulate its surrounding to avoid host immune attack suggesting a possible resistance to treatment.
Keyword(s): Cytometry, Microenvironment, Non-Hodgkin's lymphoma, T cell lymphoma
Session topic: Publication Only
Abstract: PB1941
Type: Publication Only
Background
In previous reports we have described that lack of CD26 on the surface of activated CD4+T (CD38+ ) in the microenvironment of Hodgkin lymphoma (HL) suggest a T-reg immunosuppressive activity. Other studies have shown that low expression of CD26, associated with adenosine deaminase (ADA), and the presence of CD39, ectoenzyme associated with hydrolysis of extracellular ATP, might be responsible for the generation of adenosine recognized as a major mechanism of T-reg for the suppression of anti-tumor immune responses and for successful tumour escape.
Aims
Significant amount of non-clonal cells infiltrating HL is an excellent model to analyze the para-neoplastic cellular elements of the tumor microenvironment. The scope of this study was to perform lymphocyte immunophenotyping by flow cytometry (FC) from lymph node samples suspected of lymphoma with the scope of verify biomarkers of enzymatic activity favorable to the proliferation of neoplastic cells.
Methods
We have examined the relationship between the expression of CD26 and CD39 by FC on CD4+T and measured its expression on CD4 + T subset correlating to the CD26 and CD38 in 52 samples of lymph nodes (6 HL, 30 non Hodgkin lymphoma (NHL) and 16 non malignant nodes (BN).
Results
HL samples show statically differences compared to BN in the expression of CD26 (12% vs 42%; p<0,0002), CD38 (72% vs 20%; p<0,0005), CD39 (42% vs 14% ; p<0,05). When compared to NHL there is a confirmation significance in CD26 (12% vs 37%; p<0,0007), in CD38 (72% vs 25%; p<0,0009) in contrast to CD39 (42% vs 26% ; p<0,3). Among NHL cases, there were 6 relapses, that we have compared to HL: CD26 (42% vs 12; p<0,02); CD38 (23% vs 72%; p<0,04); CD39 (30% vs 42%;p<0,7).
Summary
Data confirm the activated profile (CD38+) that distinguishes HL-infiltrating cells from NHL and BN. It is more evident in HL, but in NHL microenvironment there is a tendency to a reduction of the expression of CD26 on CD4+T cells compared with BN; this, correlated with CD39 increase, might suggests an enzymatic activity with a significant adenosine accumulation in NHL too. Although the small size of the cohort, the pattern of relapsed seems similar to HL. This mimics the regulatory microenvironments that strengthens the neoplastic cells to manipulate its surrounding to avoid host immune attack suggesting a possible resistance to treatment.
Keyword(s): Cytometry, Microenvironment, Non-Hodgkin's lymphoma, T cell lymphoma
Session topic: Publication Only
Type: Publication Only
Background
In previous reports we have described that lack of CD26 on the surface of activated CD4+T (CD38+ ) in the microenvironment of Hodgkin lymphoma (HL) suggest a T-reg immunosuppressive activity. Other studies have shown that low expression of CD26, associated with adenosine deaminase (ADA), and the presence of CD39, ectoenzyme associated with hydrolysis of extracellular ATP, might be responsible for the generation of adenosine recognized as a major mechanism of T-reg for the suppression of anti-tumor immune responses and for successful tumour escape.
Aims
Significant amount of non-clonal cells infiltrating HL is an excellent model to analyze the para-neoplastic cellular elements of the tumor microenvironment. The scope of this study was to perform lymphocyte immunophenotyping by flow cytometry (FC) from lymph node samples suspected of lymphoma with the scope of verify biomarkers of enzymatic activity favorable to the proliferation of neoplastic cells.
Methods
We have examined the relationship between the expression of CD26 and CD39 by FC on CD4+T and measured its expression on CD4 + T subset correlating to the CD26 and CD38 in 52 samples of lymph nodes (6 HL, 30 non Hodgkin lymphoma (NHL) and 16 non malignant nodes (BN).
Results
HL samples show statically differences compared to BN in the expression of CD26 (12% vs 42%; p<0,0002), CD38 (72% vs 20%; p<0,0005), CD39 (42% vs 14% ; p<0,05). When compared to NHL there is a confirmation significance in CD26 (12% vs 37%; p<0,0007), in CD38 (72% vs 25%; p<0,0009) in contrast to CD39 (42% vs 26% ; p<0,3). Among NHL cases, there were 6 relapses, that we have compared to HL: CD26 (42% vs 12; p<0,02); CD38 (23% vs 72%; p<0,04); CD39 (30% vs 42%;p<0,7).
Summary
Data confirm the activated profile (CD38+) that distinguishes HL-infiltrating cells from NHL and BN. It is more evident in HL, but in NHL microenvironment there is a tendency to a reduction of the expression of CD26 on CD4+T cells compared with BN; this, correlated with CD39 increase, might suggests an enzymatic activity with a significant adenosine accumulation in NHL too. Although the small size of the cohort, the pattern of relapsed seems similar to HL. This mimics the regulatory microenvironments that strengthens the neoplastic cells to manipulate its surrounding to avoid host immune attack suggesting a possible resistance to treatment.
Keyword(s): Cytometry, Microenvironment, Non-Hodgkin's lymphoma, T cell lymphoma
Session topic: Publication Only
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