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Gene Review:

Cd55 - CD55 antigen

Mus musculus

Synonyms: Cd55a, Complement decay-accelerating factor, GPI-anchored, Cromer blood group, DAF-GPI, Daf, ...

Miwa, T. et al., Lin, F. et al., Liu, J. et al., Cauvi, D.M. et al., Lin, F. et al., et al.

Kaminski, Kusner, Richmonds, Medof, Lin,

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Disease relevance of Cd55

Compared with wild-type mice, Daf1(-/-) mice also displayed markedly exacerbated disease progression and pathology in a T cell-dependent experimental autoimmune encephalomyelitis (EAE) model [1].
Baseline albuminuria in the Daf1(-/-), CD59a(-/-), and Daf1(-/-)CD59a(-/-) mice was 82, 83, and 139 as compared with 92 microg/mg creatinine in the WT controls (p > 0.1) [2].
We induced nephrotoxic serum (NTS) nephritis in Daf1(-/-), CD59a(-/-), Daf1(-/-)CD59a(-/-), and wild-type (WT) mice by administering NTS IgG [2].
Seven days after consuming 3% dextran sulfate sodium in their drinking water, Daf1(-/-) mice suffered markedly greater weight loss (-24.7 +/- 7.5% vs -14.2% +/- 4.9%), exhibited uniformly bloody diarrhea as compared with soft stool in control mice, developed shortened colons, and had larger spleens [3].

High impact information on Cd55

In both C57BL/6 and BALB/c mice, deficiency of the Daf1 gene, which encodes the murine homologue of human DAF, significantly enhanced T cell responses to active immunization [1].
Molecular basis of reduced or absent expression of decay-accelerating factor in Cromer blood group phenotypes [4].
To identify and characterize key transcriptional regulatory elements controlling mouse Daf1 expression, a 2.5-kb fragment corresponding to the 5' flanking region of the mouse Daf1 gene was cloned [5].
Sequence analysis showed that the mouse Daf1 promoter lacks conventional TATA and CCAAT boxes and displays a high guanine and cytosine content [5].
In contrast, electron microscopy revealed prominent podocyte foot process effacement in Daf1(-/-) mice with more widespread and severe damage in the double knockouts compared with only mild focal changes in CD59a(-/-) or WT mice [2].

Biological context of Cd55

Characterization of glycosylphosphatidylinositol-anchored decay accelerating factor (GPI-DAF) and transmembrane DAF gene expression in wild-type and GPI-DAF gene knockout mice using polyclonal and monoclonal antibodies with dual or single specificity [6].
Glomerular histology was similar in Daf1(-/-) and Daf1(+/+) mice, with essentially no infiltrating leukocytes [7].

Anatomical context of Cd55

In Daf1 knock-out mice, DAF labelling was ablated in most tissues, but strong labelling of the testis and splenic dendritic cells remained [8].
Both T and B lymphocytes and splenic macrophages express the GPI-DAF gene but the expression level is higher on B lymphocytes than on T lymphocytes [6].
Examination of the fetoplacental unit at the day 7.5 stage revealed that GPI-DAF but not the TM-DAF gene is expressed in the maternal decidua cells surrounding the trophoectoderm of the embryo [6].
By fluorescence-activated cell sorting (FACS) analysis, we found that DAF protein is present on the wild-type mouse erythrocytes and lymphocytes but no signal was detectable on the same cells of GPI-DAF gene knockout mice [6].
In contrast, only mature sperm stained positive in the GPI-DAF gene knockout mouse testis, suggesting that GPI-DAF but not the TM-DAF gene is expressed on spermatids [6].

Associations of Cd55 with chemical compounds

This contrasted with marked deposition of both C3 and C9 in Daf1(-/-)CD59a(-/-) and Daf1(-/-) mice, which was evident as early as 2 h post-NTS injection [2].
Furthermore, the regulation of uterine DAF expression by estrogen is limited to the GPI DAF gene [9].

Other interactions of Cd55

In mice, both GPI-anchored and transmembrane-anchored DAF proteins are produced, each of which can be derived from two different genes (Daf1 and Daf2) [8].

Analytical, diagnostic and therapeutic context of Cd55

Electron microscopy demonstrated markedly greater junctional damage in the Daf1(-/-) mice compared with the Daf1(+/+) littermates [10].
Molecular cloning of mouse decay accelerating factor (DAF; CD55) predicted two forms of the molecule, one transmembrane (TM) and the other glycosylphosphatidylinositol (GPI)-anchored; these are encoded by separate genes termed Daf-GPI and Daf-TM [11].
Northern blot analysis indicated that rat GPI-DAF mRNA was present in all tissues examined except for liver, while rat TM-DAF mRNA was preferentially expressed in testis [12].
At 48h, Daf1(-/-) were significantly weaker than CD59a(-/-) and WT mice, and for these mice immunohistochemistry revealed marked C9 deposition at postsynaptic junctions, radioimmunoassays showed reductions in AChR levels, and electron microscopy demonstrated massive junctional damage [13].

References

The complement inhibitory protein DAF (CD55) suppresses T cell immunity in vivo. Liu, J., Miwa, T., Hilliard, B., Chen, Y., Lambris, J.D., Wells, A.D., Song, W.C. J. Exp. Med. (2005) [Pubmed]
Respective roles of decay-accelerating factor and CD59 in circumventing glomerular injury in acute nephrotoxic serum nephritis. Lin, F., Salant, D.J., Meyerson, H., Emancipator, S., Morgan, B.P., Medof, M.E. J. Immunol. (2004) [Pubmed]
Decay-accelerating factor deficiency increases susceptibility to dextran sulfate sodium-induced colitis: role for complement in inflammatory bowel disease. Lin, F., Spencer, D., Hatala, D.A., Levine, A.D., Medof, M.E. J. Immunol. (2004) [Pubmed]
Molecular basis of reduced or absent expression of decay-accelerating factor in Cromer blood group phenotypes. Lublin, D.M., Mallinson, G., Poole, J., Reid, M.E., Thompson, E.S., Ferdman, B.R., Telen, M.J., Anstee, D.J., Tanner, M.J. Blood (1994) [Pubmed]
Constitutive expression of murine decay-accelerating factor 1 is controlled by the transcription factor sp1. Cauvi, D.M., Cauvi, G., Pollard, K.M. J. Immunol. (2006) [Pubmed]
Characterization of glycosylphosphatidylinositol-anchored decay accelerating factor (GPI-DAF) and transmembrane DAF gene expression in wild-type and GPI-DAF gene knockout mice using polyclonal and monoclonal antibodies with dual or single specificity. Miwa, T., Sun, X., Ohta, R., Okada, N., Harris, C.L., Morgan, B.P., Song, W.C. Immunology (2001) [Pubmed]
Decay-accelerating factor confers protection against complement-mediated podocyte injury in acute nephrotoxic nephritis. Lin, F., Emancipator, S.N., Salant, D.J., Medof, M.E. Lab. Invest. (2002) [Pubmed]
Tissue distribution of products of the mouse decay-accelerating factor (DAF) genes. Exploitation of a Daf1 knock-out mouse and site-specific monoclonal antibodies. Lin, F., Fukuoka, Y., Spicer, A., Ohta, R., Okada, N., Harris, C.L., Emancipator, S.N., Medof, M.E. Immunology (2001) [Pubmed]
Mouse decay-accelerating factor: selective and tissue-specific induction by estrogen of the gene encoding the glycosylphosphatidylinositol-anchored form. Song, W.C., Deng, C., Raszmann, K., Moore, R., Newbold, R., McLachlan, J.A., Negishi, M. J. Immunol. (1996) [Pubmed]
Markedly enhanced susceptibility to experimental autoimmune myasthenia gravis in the absence of decay-accelerating factor protection. Lin, F., Kaminski, H.J., Conti-Fine, B.M., Wang, W., Richmonds, C., Medof, M.E. J. Clin. Invest. (2002) [Pubmed]
Molecular and functional analysis of mouse decay accelerating factor (CD55). Harris, C.L., Rushmere, N.K., Morgan, B.P. Biochem. J. (1999) [Pubmed]
Alternative exon usage in the 3' region of a single gene generates glycosylphosphatidylinositol-anchored and transmembrane forms of rat decay-accelerating factor. Miwa, T., Okada, N., Okada, H. Immunogenetics (2000) [Pubmed]
Deficiency of decay accelerating factor and CD59 leads to crisis in experimental myasthenia. Kaminski, H.J., Kusner, L.L., Richmonds, C., Medof, M.E., Lin, F. Exp. Neurol. (2006) [Pubmed]

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