Figure 1
Figure 1. CLL mAbs bind to autoantigens. (A) I83/IGHV3-30UM IgM binding to lymph node (tonsil) thin paraffin section visualized by immunohistochemical staining. (B) I83 mAb binding to FM55M2 melanoma cells. (C) I83 mAb binding to rat aortic smooth muscle cells. (D) I83 mAb binding to Jurkat T cells. (E) HG3/IGHV1-2UM IgM binding to HepG2 cells. (F) Wa/IGHV3-30.3UM/subset-32 IgM binding to HepG2 cells. (G) AIII/IGHV4-59M IgM binding to Jurkat T cells. (H) rIGHV3-21M/subset-2 IgM binding to stomach chief cells. Secondary Ab for immunohistochemical staining was anti–IgM-biotin followed by streptavidin-HRP. Secondary Ab for immunofluorescence was anti–IgM-FITC or anti–IgM-Alexa594.

CLL mAbs bind to autoantigens. (A) I83/IGHV3-30UM IgM binding to lymph node (tonsil) thin paraffin section visualized by immunohistochemical staining. (B) I83 mAb binding to FM55M2 melanoma cells. (C) I83 mAb binding to rat aortic smooth muscle cells. (D) I83 mAb binding to Jurkat T cells. (E) HG3/IGHV1-2UM IgM binding to HepG2 cells. (F) Wa/IGHV3-30.3UM/subset-32 IgM binding to HepG2 cells. (G) AIII/IGHV4-59M IgM binding to Jurkat T cells. (H) rIGHV3-21M/subset-2 IgM binding to stomach chief cells. Secondary Ab for immunohistochemical staining was anti–IgM-biotin followed by streptavidin-HRP. Secondary Ab for immunofluorescence was anti–IgM-FITC or anti–IgM-Alexa594.

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