The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Two distinct mechanisms of antitumor activity mediated by the combination of interleukin 2 and monoclonal antibodies.

Previously we described a human B-lymphoma xenotransplantation model in which the immunotherapeutic activity of monoclonal antibodies (mAbs), directed against human B-cell antigens, can be studied. An anti-CD19 mAb of IgG2a subclass was therapeutically active by itself in this model, and its efficacy was increased by simultaneous administration of recombinant interleukin 2 (rIL-2). Immunotherapy with IgG1 or IgG2b isotype variants of an anti-CD19 mAb was ineffective if given alone. We now show that the combination of these ineffective isotype variants with rIL-2 results in significant antitumor effects, although IgG2a anti-CD19 mAb in combination with rIL-2 was therapeutically more active. In vitro studies of the effector mechanisms possibly involved in these treatment modalities indicate that the antitumor activity of IgG1 or IgG2b anti-CD19 mAbs in combination with rIL-2 may be mediated by rIL-2-induced antibody-dependent cellular cytotoxic activity of lymphocytes. The antitumor effect of IgG2a anti-CD19 mAb in combination with rIL-2 may be mediated not only by rIL-2-induced antibody-dependent cellular cytotoxic activity of lymphocytes but also by IgG2a-restricted antitumor activity of monocytes/macrophages. These results may explain the greater in vivo efficacy of treatment with rIL-2 and IgG2a subclass mAb versus treatment with rIL-2 and IgG1 or IgG2b subclass mAbs.[1]

References

 
WikiGenes - Universities