Figure 3
Reactivity of a panel of CLL rAbs with different motifs and light chains to pUL32. Blotting of different stereotypic CLL rAbs with IGHV1-69 (CLL69A, CLL69B, and CLL69D), IGHV3-21 (CLL3-21M1, CLL3-21U1, and CLL3-21U2), and IGHV4-39 (CLL4-39A) gene against lysates of CMV- and mock-infected cells (A) and lysates of pUL32- and pCDNA-transfected cells (B). A mAb specific for pUL32 (α-UL32), serum from a CMV-seronegative individual, and a CMV-seropositive individual (Se CMV− and CMV+, respectively), and a mAb specific for the human herpesvirus-6 glycoprotein 60/110 (α–HHV-6) were used as controls. Concentrations of CLL rAbs ranged between 5 and 7.5 μg/mL. Actin served as a control for protein loading.

Reactivity of a panel of CLL rAbs with different motifs and light chains to pUL32. Blotting of different stereotypic CLL rAbs with IGHV1-69 (CLL69A, CLL69B, and CLL69D), IGHV3-21 (CLL3-21M1, CLL3-21U1, and CLL3-21U2), and IGHV4-39 (CLL4-39A) gene against lysates of CMV- and mock-infected cells (A) and lysates of pUL32- and pCDNA-transfected cells (B). A mAb specific for pUL32 (α-UL32), serum from a CMV-seronegative individual, and a CMV-seropositive individual (Se CMV− and CMV+, respectively), and a mAb specific for the human herpesvirus-6 glycoprotein 60/110 (α–HHV-6) were used as controls. Concentrations of CLL rAbs ranged between 5 and 7.5 μg/mL. Actin served as a control for protein loading.

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