CD43 interferes with T-lymphocyte adhesion.

Ardman, Blair; Sikorski, Maria A.; Staunton, Donald E.

doi:10.1073/pnas.89.11.5001

Cited by 154 publications

(106 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, our results showing the lack of well developed spleen follicles, defective germinal centres and the presence of T cell-dependent areas depleted of T lymphocytes suggest the absence of the optimal lymphoid architecture required to achieve adequate antigen presentation and costimulation. In this context, our results on the expression of CD43 might be of special relevance given the adhesive features of CD43 [22][23][24]. We found fewer CD43-expressing T cells in the peripheral blood of WAS patients (where more activated/memory T lymphocytes were found) than in controls, and more CD43-expressing T lymphocytes in the spleen of WAS (where naive cells were accumulated) than in the normal individual.…”

Section: Discussionmentioning

confidence: 57%

Multiple antigens are altered on T and B lymphocytes from peripheral blood and spleen of patients with Wiskott-Aldrich syndrome

Gerwin¹,

Friedrich²,

Perez‐Atayde

et al. 1996

Clinical and Experimental Immunology

View full text Add to dashboard Cite

SUMMARYThe gene for Wiskott-Aldrich syndrome (WAS) has been recently identified and cloned, but our knowledge of downstream events affected in WAS is limited to a few leucocyte cell surface molecules. To identify cell surface molecules whose abnormal expression could contribute to the functional impairment observed in WAS B and T lymphocytes, we studied the expression of a large panel of antigens on peripheral blood lymphoid cells (PBLC) and on isolated lymphocyte subpopulations from the spleen of WAS patients. WAS T lymphocytes from peripheral blood express increased levels of the activation antigens 4F2, CD49d, CD49e, CD53 and the activation/memory marker CD45RO. In the spleen, however, WAS patients have more CD45RA CD4 and CD8 T lymphocytes than normal individuals, suggesting the selective accumulation of presumably naive cells in the WAS spleen. Interestingly, the naive phenotype of the lymphocytes that seem to accumulate in the WAS spleen is confirmed by the absence of increased expression of several activation antigens on their surface, and this correlated with their increased expression of CD43. These lymphocyte abnormalities were accompanied by an abnormal distribution of lymphocyte subsets within the spleen architecture, in particular by the lack of well developed germinal centres and T cell areas. We also found abnormal expression of CD43 and other sialyated proteins such as CDw75 and CD76, whose expression requires the action of specific sialyltransferases. This study shows that the combined impairment in cellular and humoral immunity observed in WAS is the result of multiple molecular abnormalities on the surface of WAS lymphocytes, that in turn might result in recirculation/migration anomalies.

show abstract

Section: Discussionmentioning

confidence: 57%

Multiple antigens are altered on T and B lymphocytes from peripheral blood and spleen of patients with Wiskott-Aldrich syndrome

Gerwin¹,

Friedrich²,

Perez‐Atayde

et al. 1996

Clinical and Experimental Immunology

View full text Add to dashboard Cite

show abstract

“…CD43 is important for the function of the immune system and appears to be involved in cell adhesion and cell proliferation. Owing to the structural characteristics of the extracellular domain of CD43, this molecule has both adhesive and antiadhesive properties (Ardman et al, 1992;Ostberg et al, 1996). Although there are no ligands known for the extracellular domain of CD43, ligation of CD43 causes cell signaling probably via the cytoplasmic tail of CD43.…”

Section: Introductionmentioning

confidence: 99%

Overexpression of leukocyte marker CD43 causes activation of the tumor suppressor proteins p53 and ARF

2003

View full text Add to dashboard Cite

CD43 or leukosialin is a transmembrane sialoglycoprotein, whose extracellular domain participates in cell adhesiveness and the cytoplasmic tail regulates a variety of intracellular signal transduction pathways involved in cell proliferation. CD43 is abundantly expressed on the surface of hematopoietic cells, but CD43 expression is also frequently found in the tumor cells of nonhematopoietic origin. In the early stages of some tumors, the accumulation of tumor suppressor protein p53 has been described. Here, we show that the expression of CD43 causes the induction of functionally active p53 protein.Moreover, we found that the activation of p53 by CD43 is mediated by tumor suppressor protein ARF. The coexpression of CD43 and ARF in ARF-null mouse embryonic fibroblasts resulted in programmed cell death, but that was not the case when CD43 alone was expressed in these cells. These data provide the first evidence of the connection between p53-and CD43-dependent pathways.

show abstract

“…In the case of PC, we demonstrated that charge repulsion is the main mechanism involved, because removal of sialic acid from cells overexpressing PC restores normal adhesion properties. The neuronal cell adhesion molecule N-CAM has also been shown to reduce cell-cell and cell-matrix adhesion by charge repulsion when the molecule is polysialylated (Ardman et al, 1992;Yang et al, 1992;Rutishauser and Landmesser, 1996).…”

Section: Discussionmentioning

confidence: 99%

Expression of Podocalyxin Inhibits Cell–Cell Adhesion and Modifies Junctional Properties in Madin-Darby Canine Kidney Cells

Takeda¹,

Go²,

Orlando

et al. 2000

MBoC

184

181

View full text Add to dashboard Cite

Podocalyxin is a major membrane protein of the glomerular epithelium and is thought to be involved in maintenance of the architecture of the foot processes and filtration slits characteristic of this unique epithelium by virtue of its high negative charge. However, until now there has been no direct evidence for podocalyxin's function. Podocalyxin is a type 1 transmembrane sialoprotein with an N-terminal mucin-like domain. To assess its function, we cloned rat podocalyxin and examined the effects of its expression on the cell adhesion properties of stably transfected Chinese hamster ovary (CHO)-K1 and Madin-Darby canine kidney (MDCK) cells and inducible ecdysone receptor-expressing (EcR)-CHO cells. In a cell aggregation assay, CHO-K1 cells expressing high levels of podocalyxin showed complete inhibition of cell aggregation, and MDCK transfectants showed greatly reduced aggregation (ϳ60 -80%) compared with parental cells. In EcR-CHO cells, the expression level of podocalyxin induced by increasing levels of ecdysone analogue correlated closely with the antiadhesion effect. The inhibitory effect of podocalyxin was reversed by treatment of the cells with Arthrobacter ureafaciens sialidase, indicating that sialic acid is required for inhibition of cell adhesion. Overexpression of podocalyxin also affected transepithelial resistance and the distribution of junctional proteins in MDCK cells by an unknown mechanism that may involve interaction with the actin cytoskeleton. These results provide direct evidence that podocalyxin functions as an antiadhesin that maintains an open filtration pathway between neighboring foot processes in the glomerular epithelium by charge repulsion.

show abstract

CD43 interferes with T-lymphocyte adhesion.

Cited by 154 publications

References 32 publications

Multiple antigens are altered on T and B lymphocytes from peripheral blood and spleen of patients with Wiskott-Aldrich syndrome

Multiple antigens are altered on T and B lymphocytes from peripheral blood and spleen of patients with Wiskott-Aldrich syndrome

Overexpression of leukocyte marker CD43 causes activation of the tumor suppressor proteins p53 and ARF

Expression of Podocalyxin Inhibits Cell–Cell Adhesion and Modifies Junctional Properties in Madin-Darby Canine Kidney Cells

Contact Info

Product

Resources

About