CD 10 (CALLA, common acute lymphoblastic leukemia antigen)/neutral endopeptidase 24.11 (NEP, “nkephalinase”) : molecular structure and role in regulating met-enkephalin mediated inflammatory responses

1991 ◽  
Vol 1 (2) ◽  
pp. 139-149 ◽  
Author(s):  
Margaret A. Shipp ◽  
George B. Stefano ◽  
Berta Scharrer ◽  
Ellis L. Reinherz
Keyword(s):  
Molecular Structure ◽  
Acute Lymphoblastic Leukemia ◽  
Inflammatory Responses ◽  
Lymphoblastic Leukemia ◽  
Neutral Endopeptidase ◽  
Endopeptidase 24.11 ◽  
Leukemia Antigen

CD10 (CALLA)/neutral endopeptidase 24.11 modulates inflammatory peptide- induced changes in neutrophil morphology, migration, and adhesion proteins and is itself regulated by neutrophil activation

Blood ◽  
1991 ◽  
Vol 78 (7) ◽  
pp. 1834-1841 ◽  
Author(s):  
MA Shipp ◽  
GB Stefano ◽  
SN Switzer ◽  
JD Griffin ◽  
EL Reinherz
Keyword(s):  
Substance P ◽  
Cell Surface ◽  
Enzymatic Activity ◽  
Inflammatory Responses ◽  
Lymphoblastic Leukemia ◽  
Neutral Endopeptidase ◽  
Biologically Active ◽  
Zinc Metalloprotease ◽  
Endopeptidase 24.11 ◽  
Induced Changes

Abstract The common acute lymphoblastic leukemia antigen (CALLA, CD10), which is expressed on early lymphoid progenitors and neutrophils, is the zinc metalloprotease, neutral endopeptidase 24.11 (NEP, “enkephalinase”). The CD10 cell surface enzyme is known to hydrolyze a variety of biologically active peptides including met-enkephalin, formyl-met-leu- phe (f-MLP), and substance P. These three CD10/NEP substrates induce the migration and aggregation of neutrophils, suggesting that each of the peptides can function as a mediator of neutrophil inflammatory responses. Recently, inhibition of CD10/NEP was found to reduce the concentration of metenkephalin needed to activate human and invertebrate granulocytes by several orders of magnitude. Herein we show that f-MLP and substance P induce rapid changes in neutrophil morphology, migration, and adhesion molecule expression, including upregulation of Mo1 (CD11b/CD18) and shedding of LAM-1 (also known as LECAM-1, Leu8, or TQ-1, the human homologue of murine gp100MEL14). Importantly, these coordinated changes are potentiated by inhibition of cell surface CD10/NEP enzymatic activity. Neutrophil cell surface CD10/NEP enzymatic activity is also shown to be regulated by the activation state of the cell during the time period in which the enzyme has its most pronounced effects. These results suggest that in neutrophils, CD10/NEP functions to control responsiveness to multiple inflammatory peptides.

Effects of monoclonal antibodies raised against the common acute lymphoblastic leukemia antigen on endopeptidase-24.11 activity

1992 ◽  
Vol 43 (4) ◽  
pp. 809-814 ◽  
Author(s):  
Armelle Helene ◽  
Pierre-Emmanuel Milhiet ◽  
Houda Haouas ◽  
Claude Boucheix ◽  
Ann Beaumont ◽  
...  
Keyword(s):  
Monoclonal Antibodies ◽  
Acute Lymphoblastic Leukemia ◽  
Lymphoblastic Leukemia ◽  
Endopeptidase 24.11 ◽  
The Common ◽  
Leukemia Antigen

scholarly journals CD10 (CALLA)/neutral endopeptidase 24.11 modulates inflammatory peptide- induced changes in neutrophil morphology, migration, and adhesion proteins and is itself regulated by neutrophil activation

Blood ◽  
1991 ◽  
Vol 78 (7) ◽  
pp. 1834-1841 ◽  
Author(s):  
MA Shipp ◽  
GB Stefano ◽  
SN Switzer ◽  
JD Griffin ◽  
EL Reinherz
Keyword(s):  
Substance P ◽  
Cell Surface ◽  
Enzymatic Activity ◽  
Inflammatory Responses ◽  
Lymphoblastic Leukemia ◽  
Neutral Endopeptidase ◽  
Biologically Active ◽  
Zinc Metalloprotease ◽  
Endopeptidase 24.11 ◽  
Induced Changes

The common acute lymphoblastic leukemia antigen (CALLA, CD10), which is expressed on early lymphoid progenitors and neutrophils, is the zinc metalloprotease, neutral endopeptidase 24.11 (NEP, “enkephalinase”). The CD10 cell surface enzyme is known to hydrolyze a variety of biologically active peptides including met-enkephalin, formyl-met-leu- phe (f-MLP), and substance P. These three CD10/NEP substrates induce the migration and aggregation of neutrophils, suggesting that each of the peptides can function as a mediator of neutrophil inflammatory responses. Recently, inhibition of CD10/NEP was found to reduce the concentration of metenkephalin needed to activate human and invertebrate granulocytes by several orders of magnitude. Herein we show that f-MLP and substance P induce rapid changes in neutrophil morphology, migration, and adhesion molecule expression, including upregulation of Mo1 (CD11b/CD18) and shedding of LAM-1 (also known as LECAM-1, Leu8, or TQ-1, the human homologue of murine gp100MEL14). Importantly, these coordinated changes are potentiated by inhibition of cell surface CD10/NEP enzymatic activity. Neutrophil cell surface CD10/NEP enzymatic activity is also shown to be regulated by the activation state of the cell during the time period in which the enzyme has its most pronounced effects. These results suggest that in neutrophils, CD10/NEP functions to control responsiveness to multiple inflammatory peptides.

Human glioma cell lines expressing the common acute lymphoblastic leukemia antigen (cALLa) have neutral endopeptidase activity

1989 ◽  
Vol 44 (5) ◽  
pp. 948-951 ◽  
Author(s):  
Léonard Monod ◽  
Annie-Claire Disekens ◽  
C. Victor Jongeneel ◽  
Stefan Carrel ◽  
Pierre Ronco ◽  
...  
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
Cell Lines ◽  
Glioma Cell ◽  
Lymphoblastic Leukemia ◽  
Neutral Endopeptidase ◽  
Human Glioma ◽  
Endopeptidase Activity ◽  
Glioma Cell Lines ◽  
The Common ◽  
Leukemia Antigen

scholarly journals CALLA-positive myeloma: an aggressive subtype with poor survival

Blood ◽  
1985 ◽  
Vol 66 (1) ◽  
pp. 229-232
Author(s):  
BG Durie ◽  
TM Grogan
Keyword(s):  
Bone Marrow ◽  
Acute Lymphoblastic Leukemia ◽  
Cell Lines ◽  
Median Survival ◽  
Lymphoblastic Leukemia ◽  
Myeloma Cell ◽  
Negative Group ◽  
Poor Survival ◽  
Aggressive Subtype ◽  
Leukemia Antigen

Detailed immunotyping was carried out on 21 direct myeloma bone marrow aspirates and eight human myeloma cell lines. Four previously untreated common acute lymphoblastic leukemia antigen (CALLA)-positive myeloma patients were identified and six of eight cell lines (75%) were also positive. CALLA positivity, as part of an immature B phenotype, was found to correlate with very aggressive clinical disease: median survival six months v 56 months for the CALLA-negative group.

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