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- Table of Contents
Facts about Lymphocyte function-associated antigen 3.
Ligand of the T-lymphocyte CD2 glycoprotein.
This interaction is important in mediating thymocyte interactions with thymic epithelial cells, antigen-independent and -dependent interactions of T-lymphocytes with target cells and antigen- presenting cells and the T-lymphocyte rosetting with erythrocytes.In addition, the LFA-3/CD2 interaction may prime response by both the CD2+ and LFA-3+ cells. .
Human | |
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Gene Name: | CD58 |
Uniprot: | P19256 |
Entrez: | 965 |
Belongs to: |
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No superfamily |
Ag3; CD58 antigen; CD58 antigen, (lymphocyte function-associated antigen 3); CD58 molecule; CD58; FLJ23181; FLJ43722; LFA3; LFA-3; LFA3ag3; lymphocyte function-associated antigen 3; Surface glycoprotein LFA-3
Mass (kDA):
28.147 kDA
Human | |
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Location: | 1p13.1 |
Sequence: | 1; NC_000001.11 (116500390..116571093, complement) |
[Isoform 1]: Cell membrane; Single-pass type I membrane protein.
In this article we will look at the benefits of using CD73 as a marker for minimal residual disease. We will also explore the applications of CD73 and discuss its interpretation. If you are a clinician who is considering CD73 for a clinical trial, read on to learn more. After reading this article, you will be well-equipped to start using this marker. It is a valuable tool for monitoring minimal residual disease (MRD).
The differential expression of CD73 on leukemic B cells is helpful for monitoring minimal residual disease. This marker correlates with other molecular markers of ALL relapse. It is not downregulated by treatment, and thus may be used for diagnosis and monitoring minimal residual disease. This molecule is expressed on a small percentage of memory CD8+ cells. It is also useful in the monitoring of B-ALL.
In a recent study, a number of new markers were identified. These new markers have the potential to monitor minimal residual disease in a patient's blood, including samples without LAIP. CD73 expression is stable in patients who are MRD-positive at day 33, whereas CD86, CD44, and MMP-9 are not. This makes CD73 a useful marker for MRD monitoring.
Furthermore, CD73 is a promising marker for MRD monitoring in BCP-ALL. CD73 expression increases during therapy, and the results of this study suggest that CD73 can be a useful marker to monitor minimal residual disease in these patients. This study was supported by the National Center for Research and Development. The findings are preliminary and need to be confirmed in a larger trial. So, what is CD73?
Compared to nMFI, CD73 expression is more than three times more sensitive than nMFI-a, a marker for CD73 was found to be useful in six of the nine cases. In addition to being a useful marker for monitoring minimal residual disease, it may be useful in other clinical settings as well. This marker is often acquired during treatment. However, the authors also noted that CD73 may be a useful marker for minimal residual disease in cases where chemotherapy does not cure the disease.
The study found that CD73 was the most important antigen in four out of 177 patients. This finding indicates its utility compared to CD38 and CD22, which were the other two most common markers. Furthermore, CD73's expression increased five-fold compared to CD45 and CD22. This result is encouraging and should help physicians monitor minimal residual disease. But more research is needed to determine its utility.
The objective of this study was to evaluate the role of CD73 as a surrogate marker of response in MRD and select six most effective markers to add to routine MRD panels. In the future, the value of minimal residual disease will improve greatly. There are many factors that contribute to this outcome, and it is important to know what they are. These factors help doctors monitor the treatment and select the best course of action for patients with MRD.
The development of an accurate and reliable marker for MRD monitoring should be a priority for clinicians. A reliable marker should be easy to use and affordable. There are currently two major approaches for MRD determination. One is the use of multiparametric flow cytometry (MPFC), which is fast, sensitive, and widely applicable. There are also other 5'-nucleotidases in the cytoplasm and lysosomes that are unrelated to CD73.
In this review article, the important effects of the CD58 antigen on tumor cells are outlined. These effects have important implications for T/NK cell-mediated immune response, cancer, and immunotherapy. Although the mechanisms by which CD58 suppresses tumor immune response are still unknown, the potential for new immunotherapies to inhibit cancer cell immune responses is intriguing. Further research is needed to explore the role of this immunoregulatory molecule.
Recent research has shown that the CD58 molecule has both stem-like properties and functions as an oncogene in tumor initiation. Xu et al. found that CD58 was highly expressed in CRC tumors, and that CD58-positive tumor cells were common in primary specimens. These tumor cells exhibited increased tumorigenicity in vitro, and their elevated expression facilitated self-renewal. In addition, elevated CD58 increased the activity of the Wnt/b-catenin signaling pathway. As a result, the CD58-expression of CRC tumor-initiating cells inhibited the production of Dickkopf 3, which is a degradation of Dickkopf 3. As a result, CD58 silence decreased the formation of tumor spheres and dampened the growth of CRCs.
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PMID: 3309127 by Wallner B.P., et al. Primary structure of lymphocyte function-associated antigen 3 (LFA- 3). The ligand of the T lymphocyte CD2 glycoprotein.
PMID: 3313052 by Seed B.; An LFA-3 cDNA encodes a phospholipid-linked membrane protein homologous to its receptor CD2.