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. 1999 Jun;154(6):1793–1804. doi: 10.1016/S0002-9440(10)65435-1

Figure 2.

Figure 2.

Figure 2. A and B: In situ co-localization of Ml. antigens and immunocompetent cells. Sequential sections of the lesion of an untreated MB patient (BI 4+) were double stained with the MAb to LAM (red) with either the MAb to T cell marker (anti-CD3, blue; A) or the MAb to macrophage marker (anti-CD68, blue; B). Note the intracellular presence of LAM within macrophages. Immunohistochemical double staining; magnification, ×160.

Figure 3. A and B: In situ detection of LAM and PGL-I in the course of the disease. Sequential sections of the lesion of a MB patient (1 year after the onset of the treatment, BI 2+) were stained with the MAb to LAM (A) and the MAb to PGL-I (B). C: Inset from B, showing scattered cells stained with the MAb to PGL-I. Immunoperoxidase single staining, hematoxylin counterstaining; magnification, ×40.

Figure 4.In situ detection of LAM and PGL-I in the course of the disease with RR. Sequential sections of the lesion of a MB patient with RR (BI 4+) in the course of treatment were stained with the MAb to LAM (A) and the MAb to PGL-I (B). Immunoperoxidase single staining, hematoxylin counterstaining; magnification, ×40.

Figure 5.In situ detection of LAM in the lesional skin of a MB patient with ENL after treatment. A section of the lesion of a MB patient experiencing an ENL 2 years after being released from treatment (BI 0–1+) stained with the MAb to LAM. Immunoperoxidase single staining, hematoxylin counterstaining; magnification, ×80.