ABSTRACT
Objective To explore the expression of activation-induced cytidine deaminase (AICDA) in renal tissues of patients with systemic lupus erythematosus (SLE) and its clinical significance. Methods The renal biospy tissues from 73 patients with SLE and 36 patients with primary membranous nephropathy, who underwent biopsy between Mar. 2013 to Jun. 2017 in Central South University Xiangya School of Medicine Affiliated Haikou Hospital, were collected. Immunohistochemical method was used to detect the expression of AICDA in renal tissues. The correlations between the expression level of AICDA and the clinicopathological parameters, including pathological classification, system damage, SLE disease activity index (DAI) score and treatment outcome of SLE patients were analyzed. Results The expression level of AICDA in renal tissues of SLE patients was significantly higher than that of primary membrane nephropathy patients (6.12±2.47 vs 3.33±1.91, P0.05). The expression levels of AICDA were significantly higher in renal tissues of SLE patients with oral ulcer, interstitial pneumonia, nervous system damage, arthritis, blood system damage or serositis than those in the patients without above symptoms (7.02±2.14 vs 4.17±1.97, 7.86±2.39 vs 4.98±1.76, 9.83±1.34 vs 5.39±1.92, 6.88±2.04 vs 2.93±1.21, 7.51±1.81 vs 3.70±1.23, and 7.29±2.33 vs 5.34±2.29; all P0.05). Conclusion AICDA is related to the occurrence and development of SLE, and it is expected to bring new targets for the treatment of SLE.
ABSTRACT
Since its first description by Denis Burkitt, endemic Burkitt's lymphoma (BL), the most common childhood cancer in sub-Saharan Africa, has led scientists to search for clues to the origins of this malignancy. The discovery of Epstein-Barr virus (EBV) in BL cells over 50 years ago led to extensive sero-epidemiology studies and revealed that rather than being a virus restricted to areas where BL is endemic, EBV is ubiquitous in the world's population with an estimated greater than 90% of adults worldwide infected. A second pathogen, Plasmodium falciparum (P. falciparum) malaria is also linked to BL. In this review, we will discuss recent studies that indicate a role for P. falciparum malaria in dysregulating EBV infection, and increasing the risk for BL in children living where P. falciparum malaria transmission is high.
Desde la primera descripción por Denis Burkitt, el linfoma de Burkitt (LB) endémico -el tipo de cáncer pediátrico más común en el África subsahariana- ha guiado a los científicos a investigar este padecimiento en la búsqueda de claves para entender sus orígenes. El descubrimiento desde hace 50 años del virus de Epstein-Barr (VEB) en el LB ha conducido a extensos estudios sero-epidemiológicos y ha revelado que, más que ser un virus restringido a áreas donde el LB es endémico, el VEB es ubicuo en la población mundial, con un estimado mayor del 90% de adultos infectados a escala global. Un segundo agente patógeno se ha ligado al LB, el Plasmodium falciparum (P. falciparum) malaria. En esta revisión se discuten los estudios recientes que indican el papel de P. falciparum malaria en la desregulación de la infección por VEB y en el aumento del riego del LB en niños que viven en regiones con alta transmisión de P. falciparum malaria.
ABSTRACT
Objective To investigate the characteristics of activation-induced cytidine deaminase (AID) expression level in de novo acute leukemia (AL) patients, chronic myeloid leukemia chronic phase (CML-CP), chronic myeloid leukemia blastic crisis (CML-BC) patients and leukemia cell lines. Methods The expression level of AID mRNA was measured in 89 cases of newly-diagnosed acute lymphoblastic leukemia (ALL) patients, 79 cases of de novo acute myeloid leukemia (AML) patients, 5 cases of CML-BC patients, 5 cases of CML-CP patients and leukemia cell lines NB4, THP-1, KG-1, Raji, K562 by real-time quantitative reverse transcriptase polymerase chain reaction (RT-PCR), bone marrow mononuclear cells of 16 normal healthy donors were used as the control group. Results The expression levels of AID mRNA in 89 cases of ALL and 79 cases of AML were 0.006-7 463.175 and 0.005-69.107, the median expression levels were 3.785 and 1.812, the expression level of AID mRNA in the normal control group was 0.146-4.707, and the median expression level was 1.483, respectively. The AID expression levels of ALL, B-ALL, Burkitt leukemia, M4 patients and Raji cells were significantly higher than those of the normal control group (all P <0.05). Nevertheless, the AID mRNA expression levels of M3 patients and NB4, KG-1 cells were lower than those of the normal control group (all P <0.05). Furthermore, the AID mRNA expression levels of K562 cell were strikingly higher than that of the CML-CP patients (P<0.001), so were those of CML-BC, chronic myeloid leukemia myeloid blast crisis (CML-MBC), chronic myeloid leukemia lymphoblastic blast crisis (CML-LBC) patients. Conclusion AID gene shows high expression level in B-ALL, Burkitt leukemia and M4, low expression level in M3 and KG-1 cells, and obvious high expression level in CML-BC.
ABSTRACT
Objective To explore the relationship between activation-induced cytidine deaminase (AID) expression and melanoma invasion, metastasis and prognosis, and to evaluate the clinical significance of AID. Methods An immunohistochemical study was conducted to detect the expression of AID in paraffin-embedded tissue sections from 80 cases of melanoma and 23 cases of pigmented nevus. The relationship between the expression of AID and clinicopathological and biological features of melanoma was analyzed. Results The expression rate of AID was significantly higher in melanoma than in pigmented nevus tissue specimens(53.75%(43/80)vs. 13.04%(3/23), P 0.05). Of 19 melanoma specimens with BRAF mutations, 17 expressed AID, including all the 15 melanoma specimens with the BRAFV600E mutation. Conclusions AID may induce BRAF mutations in melanoma, participate in melanoma invasion and metastasis, and be correlated with melanoma prognosis.
ABSTRACT
Activation-induced cytidine deaminase (AID) is an enzyme that is predominantly expressed in germinal center B cells and plays a pivotal role in immunoglobulin class switch recombination and somatic hypermutation for antibody (Ab) maturation. These two genetic processes endow Abs with protective functions against a multitude of antigens (pathogens) during humoral immune responses. In B cells, AID expression is regulated at the level of either transcriptional activation on AID gene loci or post-transcriptional suppression of AID mRNA. Furthermore, AID stabilization and targeting are determined by post-translational modifications and interactions with other cellular/nuclear factors. On the other hand, aberrant expression of AID causes B cell leukemias and lymphomas, including Burkitt's lymphoma caused by c-myc/IgH translocation. AID is also ectopically expressed in T cells and non-immune cells, and triggers point mutations in relevant DNA loci, resulting in tumorigenesis. Here, I review the recent literatures on the function of AID, regulation of AID expression, stability and targeting in B cells, and AID-related tumor formation.
Subject(s)
B-Lymphocytes , Burkitt Lymphoma , Cell Transformation, Neoplastic , Cytidine , Cytidine Deaminase , DNA , Genetic Phenomena , Germinal Center , Hand , Immunity, Humoral , Immunoglobulins , Leukemia, B-Cell , Lymphoma , Point Mutation , Protein Processing, Post-Translational , Recombination, Genetic , RNA, Messenger , T-Lymphocytes , Transcriptional ActivationABSTRACT
Activation-induced cytidine deaminase (AID) is an enzyme that is predominantly expressed in germinal center B cells and plays a pivotal role in immunoglobulin class switch recombination and somatic hypermutation for antibody (Ab) maturation. These two genetic processes endow Abs with protective functions against a multitude of antigens (pathogens) during humoral immune responses. In B cells, AID expression is regulated at the level of either transcriptional activation on AID gene loci or post-transcriptional suppression of AID mRNA. Furthermore, AID stabilization and targeting are determined by post-translational modifications and interactions with other cellular/nuclear factors. On the other hand, aberrant expression of AID causes B cell leukemias and lymphomas, including Burkitt's lymphoma caused by c-myc/IgH translocation. AID is also ectopically expressed in T cells and non-immune cells, and triggers point mutations in relevant DNA loci, resulting in tumorigenesis. Here, I review the recent literatures on the function of AID, regulation of AID expression, stability and targeting in B cells, and AID-related tumor formation.
Subject(s)
B-Lymphocytes , Burkitt Lymphoma , Cell Transformation, Neoplastic , Cytidine , Cytidine Deaminase , DNA , Genetic Phenomena , Germinal Center , Hand , Immunity, Humoral , Immunoglobulins , Leukemia, B-Cell , Lymphoma , Point Mutation , Protein Processing, Post-Translational , Recombination, Genetic , RNA, Messenger , T-Lymphocytes , Transcriptional ActivationABSTRACT
The second step of immunoglobulin gene alteration consists of somatic hypermutation and class switch recombination. 80th are regulated by activation-induced cytidine deaminase (AID). Methods: Study on possible application of class switch recombination assays for immunoglobulin gene alteration via AID. Cell based assays using AID B lymphocyte and NIH3T3 cell carrying switch substrate; gene transfer using retrovirus system; FACS analysis; PCR and ELISA. Results: DNA sequencing for S region and gamma1CT are the most sensitive and accurate assays. However, gamma1CT assay seemed to be more reliable and applicable. Others are accurate assays but less applicable. Conclusion: gamma1CT determination is the best class switch recombination assay for immunoglobulin gene alteration via AID.