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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

CD52 molecule

CD52, CD52 antigen, CDw52
glycosylphosphatidylinositol (GPI)-anchored cell surface antigen [RGD, Feb 2006] (from NCBI)
Top mentioned proteins: CD20, HAD, CAN, CD4, CD45
Papers using CD52 antibodies
Preferential migration of T regulatory cells induced by IL-16
Supplier
Wood Kathryn J et al., In European Journal of Immunology, 2006
... ), CD52-transgenic CP1-CBA.Ca (H-2 ...
Identification of Regulatory T Cells in Tolerated Allografts
Supplier
Waldmann Herman et al., In The Journal of Experimental Medicine, 2001
... ), human-CD52 transgenic CP1-CBA/Ca (H-2 ...
Papers on CD52
Modern Therapies for Idiopathic Inflammatory Myopathies (IIMs): Role of Biologics.
New
Aggarwal et al., Pittsburgh, United States. In Clin Rev Allergy Immunol, Feb 2016
Other potential novel therapies include alemtuzumab (a humanized monoclonal antibody which binds CD52 on B and T lymphocytes), fingolimod (a sphingosine 1-phosphate receptor modulator that traps T lymphocytes in the lymphoid organs), eculizumab, and basiliximab.
Cancer immunotherapy in veterinary medicine: Current options and new developments.
Review
New
Dow et al., Fort Collins, United States. In Vet J, Jan 2016
In addition, caninized monoclonal antibodies targeting CD20 and CD52 just recently received either full (CD20) or conditional (CD52) licensing by the United States Department of Agriculture for clinical use in the treatment of canine B-cell and T-cell lymphomas, respectively.
Alemtuzumab in T-cell large granular lymphocytic leukaemia: interim results from a single-arm, open-label, phase 2 study.
New
Scheinberg et al., Bethesda, United States. In Lancet Haematol, Jan 2016
We aimed to explore the activity and safety of alemtuzumab, an anti-CD52 monoclonal antibody, in patients with T-LGL.
Alemtuzumab and CHOP Chemotherapy for the Treatment of Aggressive Histology Peripheral T Cell Lymphomas: A Multi-Center Phase I Study.
New
Crump et al., Toronto, Canada. In Clin Lymphoma Myeloma Leuk, Jan 2016
PATIENTS AND METHODS: Adult patients with untreated CD52-positive (CD52(+)) PTL were enrolled in a phase I trial.
Potential therapeutic targets in plasma cell disorders: A flow cytometry study.
New
Hundemer et al., Heidelberg, Germany. In Cytometry B Clin Cytom, Jan 2016
We retrospectively analyzed the expression of CD20, CD22, CD27, CD30, CD38, CD52, CD81, CD138 and SLAMF7 on PCs by flow cytometry in 103 patients with PC disorders.
The use of novel monoclonal antibodies in the treatment of acute lymphoblastic leukemia.
New
DeAngelo, Boston, United States. In Hematology Am Soc Hematol Educ Program, Jan 2016
Several approaches have been used to target antigens, including cluster of differentiation (CD) 19, CD20, CD22, and CD52, on the surface of the malignant lymphoblast with striking efficacy.
World Health Organization-defined eosinophilic disorders: 2015 update on diagnosis, risk stratification, and management.
Review
New
Gotlib, Stanford, United States. In Am J Hematol, Nov 2015
Although clinical trials have been performed with anti IL-5 (mepolizumab) and anti-CD52 (alemtuzumab) antibodies, their therapeutic role in primary eosinophilic diseases and HES has yet to be established.
Future perspectives in target-specific immunotherapies of myasthenia gravis.
Review
New
Dalakas, Philadelphia, United States. In Ther Adv Neurol Disord, Nov 2015
Novel biological agents currently on the market, directed against the following molecular pathways, are relevant and specific therapeutic targets that can be tested in MG: (a) T cell intracellular signaling molecules, such as anti-CD52, anti-interleukin (IL) 2 receptors, anti- costimulatory molecules, and anti-Janus tyrosine kinases (JAK1, JAK3) that block the intracellular cascade associated with T-cell activation; (b) B cells and their trophic factors, directed against key B-cell molecules; (c) complement C3 or C5, intercepting the destructive effect of complement-fixing antibodies; (d) cytokines and cytokine receptors, such as those targeting IL-6 which promotes antibody production and IL-17, or the p40 subunit of IL-12/1L-23 that affect regulatory T cells; and (e) T and B cell transmigration molecules associated with lymphocyte egress from the lymphoid organs.
[ALEMTUZUMAB: BENEFITS AND CHALLENGES OF A NEW THERAPY IN MULTIPLE SCLEROSIS].
Review
New
Csépány et al., In Ideggyogy Sz, Jun 2015
The humanized monoclonal antibody against CD52, alemtuzumab has been approved in Europe for the treatment of MS, which results in long-term depletion of B and T cells due to complement- and antibody-mediated cytotoxicity.
Alemtuzumab in Multiple Sclerosis: Mechanism of Action and Beyond.
Review
Meuth et al., Münster, Germany. In Int J Mol Sci, 2014
Alemtuzumab is a humanized monoclonal antibody against CD52 (cluster of differentiation 52) and is approved for the therapy of relapsing-remitting multiple sclerosis.
T cell regulation mediated by interaction of soluble CD52 with the inhibitory receptor Siglec-10.
Impact
Harrison et al., Australia. In Nat Immunol, 2013
We found that human and mouse antigen-activated T cells with high expression of the lymphocyte surface marker CD52 suppressed other T cells.
Alemtuzumab for patients with relapsing multiple sclerosis after disease-modifying therapy: a randomised controlled phase 3 trial.
Impact
CARE-MS II investigators et al., Cambridge, United Kingdom. In Lancet, 2012
BACKGROUND: The anti-CD52 monoclonal antibody alemtuzumab reduces disease activity in previously untreated patients with relapsing-remitting multiple sclerosis.
Alemtuzumab versus interferon beta 1a as first-line treatment for patients with relapsing-remitting multiple sclerosis: a randomised controlled phase 3 trial.
Impact
CARE-MS I investigators et al., Cleveland, United States. In Lancet, 2012
BACKGROUND: The anti-CD52 monoclonal antibody alemtuzumab reduced disease activity in a phase 2 trial of previously untreated patients with relapsing-remitting multiple sclerosis.
The N-linked carbohydrate moiety of male reproductive tract CD52 (mrt-CD52) interferes with the complement system via binding to C1q.
GeneRIF
Komori et al., Nishinomiya, Japan. In J Reprod Immunol, 2012
carbohydrate moiety of sperm protein interferes with the complement system via binding to C1q
Alemtuzumab in combination with methylprednisolone is a highly effective induction regimen for patients with chronic lymphocytic leukemia and deletion of TP53: final results of the national cancer research institute CLL206 trial.
Impact
Hillmen et al., Liverpool, United Kingdom. In J Clin Oncol, 2012
In contrast, TP53 defects are not associated with resistance to the anti-CD52 monoclonal antibody alemtuzumab or methylprednisolone.
CT60 single-nucleotide polymorphism as a surrogate marker for donor lymphocyte infusion outcome after allogeneic cell transplantation for acute leukemia.
GeneRIF
Finke et al., Freiburg, Germany. In Bone Marrow Transplant, 2012
CT60 single-nucleotide polymorphism of CTLA4 is a surrogate marker for donor lymphocyte infusion outcome after allogeneic cell transplantation for acute leukemia
Targeting immune dysregulation in myelodysplastic syndromes.
Impact
Sloand et al., Bethesda, United States. In Jama, 2011
After treatment with a clinical protocol using alemtuzumab, an anti-CD52 antibody, her blood cell counts returned to normal and she has remained in complete remission for more than 2 years of follow-up.
CD52 expression is induced in the mouse uterus at the time of embryo implantation.
GeneRIF
Koyama et al., Nishinomiya, Japan. In J Reprod Immunol, 2009
expression is induced in the mouse uterus at the time of embryo implantation
Therapeutic implications of variable expression of CD52 on clonal cytotoxic T cells in CD8+ large granular lymphocyte leukemia.
GeneRIF
Maciejewski et al., Cleveland, United States. In Haematologica, 2009
Clonal large granular lymphocytes exhibited decreased CD52 expression post-therapy in patients refractory to treatment.
CD52 gene polymorphism and its potential effect on the response to alemtuzumab in renal transplant recipients.
GeneRIF
Czekalski et al., Poznań, Poland. In Ann Acad Med Stetin, 2008
Our bioinformatics findings suggest that CD52 polymorphism may affect the efficiency of GPI anchor formation and thus may indirectly alter the response to anti-CD52 agents like alemtuzumabin renal transplantation.
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