Disease relevance of Cd24a

• Functional analysis of a 0.6-kilobase DNA fragment containing these elements fused to the CAT reporter gene in transient transfection experiments showed activity in both HSA expressing and non-expressing cell lines with a strength similar to that of the herpes-simplex virus-thymidine kinase promoter [1].
• We show that CD28/B7 and HSA provide two alternative costimulatory pathways for induction of immunological memory to influenza virus [2].
• Thus, identification of HSA as a novel checkpoint, even after activation and expansion of self-reactive T cells, provides a novel approach for immunotherapy of autoimmune neurologic diseases, such as multiple sclerosis [3].
• Reconstitution of SCID and BALB/c-nu/nu mice with HSA transgenic marrow indicated that the perturbations in B lymphopoiesis were not caused by a defective marrow microenvironment or by abnormal T cells [4].
• To examine whether the co-stimulatory signal provided by HSA can induce an anti-tumor immune response, we have transfected HSA cDNA into the murine melanoma cell line K1735M2, and examined the ability of this transfected cell line to induce tumor-specific T cell responses [5].

High impact information on Cd24a

• We have identified a very early stage of B lineage cells in the CD45R (B220)+CD24 (HSA) pre-pro-B fraction of mouse bone marrow delineated by expression of AA4.1, a molecule found on stem cells and early B lineage cells [6].
• These results demonstrate that CD28-independent induction of T helper cells and Ig class-switches requires costimulation by the HSA [7].
• Furthermore, our results revealed that B7 is essential for the generation of effector T cells from either naive or memory T cells, while HSA is not necessary for the generation of effector T cells [2].
• Taken together, these data implicate HSA as a potent negative regulator of B cell development and activation [8].
• We have recently demonstrated a significant reduction in pro-B and pre-B lymphocytes in transgenic mice that overexpress HSA [8].

Chemical compound and disease context of Cd24a

• N-glycans of the mouse glycoprotein HSA and its human analogue CD24 from lymphoblastoma, neuroblastoma and astrocytoma cell lines as well as from mouse brain homogenate were analysed and compared to each other and to the N-glycosylation pattern of total glycoproteins from mouse and human brain [9].
• To test this hypothesis, immune complex glomerulonephritis was induced in C57BL/6 mice by intraperitoneal injections of horse spleen apoferritin and lipopolysaccharide (HSA/LPS) [10].
• In low-affinity mice fed the normal protein diet, this resulted in impairment of renal function, deposition of immunoglobulin, C3 and HSA in the glomeruli, high levels of circulating antigen-antibody complexes and death from apparent renal failure in 50% of the animals [11].

Biological context of Cd24a

• In addition, sequence and methylation analysis of the Cd24a promoter revealed characteristics of both "housekeeping" and tissue-specific promoters, including a methylation-free, HpaII tiny fragment (HTF) island, multiple putative SP1 and AP-2 consensus binding sites, and a TATA box [1].
• To test whether the CD28-independent induction of Ig class switches requires costimulation by the heat-stable antigen (HSA), we compared T helper cell induction and antibody response in mice deficient for either HSA, CD28, or both genes [7].
• Thus, all homologous loci from HSA 21 that have been studied in the cow are on a single chromosome [12].
• When infected with the malarial parasite Plasmodium chabaudi chabaudi, the levels of parasite-bearing erythrocytes in HSA-deficient mice were also significantly elevated, but the mice were able to clear the infection with kinetics similar to wild-type mice and were immune to a second challenge [13].
• Thus, apart from alterations in erythrocytes and a mild block in B-cell development, the regulated expression of HSA appears to be dispensable for the maturation and functioning of those cell lineages that normally express it [13].

Anatomical context of Cd24a

• Our data suggest that Ptn and Cd24a may be genetic markers associated with salivary gland tumorigenesis and/or progression [14].
• Heat-stable antigen is a costimulatory molecule for CD4 T cell growth [15].
• Altered erythrocytes and a leaky block in B-cell development in CD24/HSA-deficient mice [13].
• Terminally differentiated lymphocytes, as well as most myeloid lineages, are negative for HSA [13].
• We also observed that erythrocytes are altered in HSA-deficient mice [13].

Associations of Cd24a with chemical compounds

• The heat stable antigen (HSA, or murine CD24) is a glycosyl phosphatidylinositol-linked surface glycoprotein expressed on immature cells of most, if not all, major hematopoietic lineages, as well as in developing neural and epithelial cells [13].
• The MRBC membrane protein recognized by R13 (R13-Ag) can be purified by loading the butanol-extracted MRBC membrane solution on a R13-conjugated Cellulofine column in the presence of 0.1% CHAPS followed by elution with 1% CHAPS [16].
• Latex beads coated with purified nectadrin aggregated and the rate of their aggregation depended on the molecular form of nectadrin, with the larger form being more potent than the smaller one in mediating bead aggregation [17].
• Nectadrin thus appears to be a self-binding cell adhesion molecule of a structurally novel type in that its extensive glycan structures may be implicated in mediating cell adhesion [17].
• CML was also formed when glucose, preincubated with ONOO(-), was incubated with HSA but was completely inhibited by aminoguanidine, a trapping reagent for alpha-oxoaldehydes [18].

Physical interactions of Cd24a

• Treatment of HSA with OSGE significantly reduced binding of both P-selectin and I [19].

Regulatory relationships of Cd24a

• To study the role of the murine heat-stable Ag (HSA) in lymphocyte maturation, we generated transgenic mice in which the HSA cDNA was under the transcriptional control of the TCR V beta promoter and Ig mu enhancer [4].

Other interactions of Cd24a

• Anti-Forssman, Mac-1, Ia, and HSA antibodies were used to eliminate nonhematopoietic progenitors [20].
• Heat-stable antigen (mouse CD24) in the brain: dual but distinct interaction with P-selectin and L1 [19].
• Western blot analysis of splenocyte, thymocyte, bone marrow cell and erythrocyte detergent extracts revealed that LR-1 reacted with glycoforms of HSA of known molecular weights (30-55 kD) [21].
• Here we show that the brain HSA is associated with N- and O-linked oligosaccharide moieties and decorated with the HNK-1 sulfated carbohydrate epitope [19].
• Differential, LFA-1-sensitive effects of antibodies to nectadrin, the heat-stable antigen, on B lymphoblast aggregation and signal transduction [22].

Analytical, diagnostic and therapeutic context of Cd24a

• Adoptive transfer studies demonstrate that both T cells and non-T cells must express HSA in order for the pathogenic T cells to execute their effector function [3].
• Fluorescence-activated cell sorting (FACS) analysis of the cells 24 hours later showed 21% to 41% (mean, 27%) of those that were still CD34+ to have acquired the ability to express HSA [23].
• Here, acquisition of 275 kb of mouse genomic sequence from this region and comparative sequence analysis with HSA 21 and HSA 22 narrowed the junction from 380 kb to 18 kb [24].
• The stable, covalently cross-linked complexes with NAP7.0 . HSA and NAP12.9 . HSA were prepared and separated into complexes with varying degrees of lattice by sequential steps of gel filtration [25].
• Using an HIV-1 strain engineered to express the murine HSA heat-stable antigen surface marker, we explored the relationship between HIV-1 expression and CD4(+) cell resurgence kinetics in HIV-1-depleted SCID-hu implants following drug therapy [26].

References