Research Topics
Species | K A GeldermanSummaryAffiliation: Leiden University Medical Center Country: The Netherlands Publications
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Detail Information
Publications
Enhancement of the complement activating capacity of 17-1A mAb to overcome the effect of membrane-bound complement regulatory proteins on colorectal carcinomaKyra A Gelderman
Department of Pathology, Leiden University Medical Center, Leiden, The Netherlands
Eur J Immunol 32:128-35. 2002..Therefore, 17-1A conjugates and anti-17-1A / EpCAM*anti-CD55 bispecific mAb may be promising immunotherapeutic agents for patients with colorectal cancer...
The inhibitory effect of CD46, CD55, and CD59 on complement activation after immunotherapeutic treatment of cervical carcinoma cells with monoclonal antibodies or bispecific monoclonal antibodiesKyra A Gelderman
Department of Pathology, Leiden University Medical Center, Leiden, The Netherlands
Lab Invest 82:483-93. 2002..These results demonstrate that when tumor-associated antigens are expressed in adequate amounts, bispecific mAbs in vivo may be potent immunotherapeutic agents to enhance an inflammatory reaction at the tumor site...
Membrane-bound complement regulatory proteins inhibit complement activation by an immunotherapeutic mAb in a syngeneic rat colorectal cancer modelK A Gelderman
Department of Pathology, Leiden University Medical Center, L1 Q, Albinusdreef 2, P O Box 9600, 2300 RC Leiden, The Netherlands
Mol Immunol 40:13-23. 2003..The results indicate the suitability of this syngeneic animal model for studying the effects of mAb immunotherapy. However, the effect of mCRP on tumor cells need to be overcome, e.g. by the use of mAb against tumor antigens and mCRP...
Cytokines affect resistance of human renal tumour cells to complement-mediated injuryV T Blok
Department of Pathology, Leiden University Medical Center, Leiden, The Netherlands
Scand J Immunol 57:591-9. 2003..This suggests that clinical immunotherapy, consisting of treatment with cytokines and MoAb, may induce either up- or downregulation of CD55 or CD59 and thus affect the effectiveness of immunotherapy with MoAb...
CD55 expression patterns on intestinal neuronal tissue are divergent from the brainK A Gelderman
Department of Pathology, Leiden University Medical Centre, Leiden, The Netherlands
Gut 53:507-13. 2004..CD55, produced by neuronal cells, attached to elastic fibres surrounding the plexuses is proposed to protect the CD55 negative glial cells within plexuses...
Cross-linking tumor cells with effector cells via CD55 with a bispecific mAb induces beta-glucan-dependent CR3-dependent cellular cytotoxicityKyra A Gelderman
Department of Pathology, Leiden University Medical Center, Leiden, The Netherlands
Eur J Immunol 36:977-84. 2006....
Tumor-specific inhibition of membrane-bound complement regulatory protein Crry with bispecific monoclonal antibodies prevents tumor outgrowth in a rat colorectal cancer lung metastases modelKyra A Gelderman
Department of Pathology, Leiden University Medical Center, The Netherlands
Cancer Res 64:4366-72. 2004....
Complement function in mAb-mediated cancer immunotherapyKyra A Gelderman
Department of Pathology L1-Q, Leiden University Medical Center, Postbox 9600, 2300 RC Leiden, The Netherlands
Trends Immunol 25:158-64. 2004
Beta-glucan enhanced killing of renal cell carcinoma micrometastases by monoclonal antibody G250 directed complement activationCornelis F M Sier
Department of Pathology, Leiden University Medical Center, Leiden, The Netherlands
Int J Cancer 109:900-8. 2004..For CACC the presence of CR3-priming beta-glucan seems to be obligatory. In vivo, bi-MAb may be more effective as therapeutic agent due to its increased C5a generating properties...
Complement production and regulation by dendritic cells: molecular switches between tolerance and immunityCees van Kooten
Department of Nephrology, Leiden University Medical Center, Leiden, The Netherlands
Mol Immunol 45:4064-72. 2008..We will discuss the role of C1q, C3, as well as complement regulators in DC biology...
Inhibiting complement regulators in cancer immunotherapy with bispecific mAbsKyra A Gelderman
Department of Medical Inflammation Research, Lund University, BMC I 11, 221 84 Lund, Sweden
Expert Opin Biol Ther 5:1593-601. 2005..Clinical results will probably increase with such bi-mAbs compared with monovalent antitumour mAbs. In this review the feasibility of this approach is discussed...
Lack of reactive oxygen species breaks T cell tolerance to collagen type II and allows development of arthritis in miceMalin Hultqvist
Section for Medical Inflammation Research, Lund University, Lund, Sweden
J Immunol 179:1431-7. 2007..This is important as we, for the first time, can follow the effect of ROS on molecular mechanisms where T cells are responsible for either protection or promotion of arthritis depending on the level of oxygen species produced...
C4b-binding protein and factor H compensate for the loss of membrane-bound complement inhibitors to protect apoptotic cells against excessive complement attackLeendert A Trouw
Department of Laboratory Medicine, University Hospital Malmo, 5 20502 Malmö, Sweden
J Biol Chem 282:28540-8. 2007..In conclusion, during late apoptosis, cells acquire fluid phase complement inhibitors that compensate for the down-regulation of m-C-Reg and protect against excessive complement activation and lysis...
Macrophages suppress T cell responses and arthritis development in mice by producing reactive oxygen speciesKyra A Gelderman
Section of Medical Inflammation Research, Lund University, Lund, Sweden
J Clin Invest 117:3020-8. 2007..In conclusion, macrophage-derived ROS play a role in T cell selection, maturation, and differentiation, and also a suppressive role in T cell activation, and thereby mediate protection against autoimmune diseases like arthritis...
Generation and characterization of a novel anti-rat CD40L antibody with inhibitory activities in vitro and in vivoAnnelein M Stax
Department Nephrology, Leiden University Medical Center, Leiden, The Netherlands
J Immunol Methods 335:46-52. 2008..Elucidating the effect of AS1 in various rat models for human diseases will provide more insight into blocking the CD40-CD40L interaction as a therapeutic strategy to prevent human diseases...
