© 2001 American Heart Association, Inc.
Correction
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