We published “Inhibition of Arteriosclerosis by T-Cell Depletion in Normocholesterolemic Rabbits Immunized With Heat Shock Protein 65” (Arterioscler Thromb Vasc Biol. 1998;19:1905-1911) under the consideration that treatment of normocholesterolemic rabbits with a monoclonal antibody against rabbit T-cells prevents the development of arteriosclerosis after immunization with mycobacterial heat shock protein 65. The antibody used for this study was produced from the hybridoma line L11/135 obtained from the American Type Culture Collection (ATCC-No. TIB 188). In the ATCC specification, this hybridoma was described as producing antibodies reactive with rabbit T-cells. In the reference on this clone given in the ATCC specification sheet,1 a panel of six monoclonal antibodies used against cell surface glycoproteins of a rabbit T-lymphocyte line was studied. This paper explicitly states that in functional studies only the L11/135-bearing cells responded to the T-cell mitogens concanavalin A and phytohemagglutinin and to allogenic splenocytes.
However, we became aware recently that this antibody, defined as pan-T-specific, recognized the equivalent of CD43/leukosialin,2 an antigen that is strongly expressed by all T-cells, but also weakly stains monocytes and macrophages. Although the experimental data that we presented (ie, the severe quantitative and functional suppression of T-cells in the antibody-treated animals) are solid and reproducible, we are at present not able to assign the atherosclerosis-inhibiting effect to either a depletion of T-cells or the inhibition of the adhesion to and subsequent transmigration of monocytes through the vascular endothelium.3 CD3 and CD43 are jointly present in a large complex in a mild detergent lysate of T-cells, and it is suggested to add this as a co-stimulatory molecule in CD3/T-cell receptor signalling.4 Unfortunately, a pure anti-rabbit-CD3 monoclonal antibody that binds to extra cellular domains of the CD3-complex and can therefore be used for in vivo experiments is not available. We apologize for any confusion this may have caused.
Bernhard Metzler, Manuel Mayr,
Hermann Dietrich, Mahauir Singh,
Evelyn Wiebe, Qingbo Xu, George Wick
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