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Anti-CD43 inhibition of T cell homing.

McEvoy LM, Sun H, Frelinger JG, Butcher EC - J. Exp. Med. (1997)

Bottom Line: We selected antilymphocyte monoclonal antibodies (mAbs) for inhibition of lymphocyte binding in vitro to lymph node high endothelial venules (HEV), specialized vessels that support lymphocyte recruitment into lymph nodes. mAb L11 blocks T cell binding to lymph node and Peyer's patch HEV and inhibits T cell extravasation from the blood into organized secondary lymphoid tissues.The L11 antigen is CD43, a sialomucin implicated in vitro in regulation of lymphocyte activation, whose expression is often dysregulated in the Wiskott-Aldrich syndrome.CD43 represents a novel target for experimental and therapeutic manipulation of lymphocyte traffic and may help regulate T cell distribution in vivo.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology, Stanford University, California 94305, USA.

ABSTRACT
The homing of lymphocytes from the blood is controlled by specialized processes of lymphocyte-endothelial cell interaction. Interference with these processes offers the potential to manipulate lymphocyte traffic, and thus to modulate normal and pathologic immune and inflammatory responses. We selected antilymphocyte monoclonal antibodies (mAbs) for inhibition of lymphocyte binding in vitro to lymph node high endothelial venules (HEV), specialized vessels that support lymphocyte recruitment into lymph nodes. mAb L11 blocks T cell binding to lymph node and Peyer's patch HEV and inhibits T cell extravasation from the blood into organized secondary lymphoid tissues. In contrast, L11 has no effect on lymphocyte binding to purified vascular ligands for L-selectin, alpha4beta7, or LFA-1, suggesting that it inhibits by a novel mechanism. The L11 antigen is CD43, a sialomucin implicated in vitro in regulation of lymphocyte activation, whose expression is often dysregulated in the Wiskott-Aldrich syndrome. CD43 represents a novel target for experimental and therapeutic manipulation of lymphocyte traffic and may help regulate T cell distribution in vivo.

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L11 antigen is CD43. L11 (left), but not control mAb (right),  stained CD43-transfected CHO-P cells. CHO-P cells were transfected  with mouse CD43 or mouse MAdCAM-1 cDNA and stained with L11  mAb or control mAb MECA367 (anti–mouse MAdCAM-1). MECA367  recognized MAdCAM-1 transfectants (not shown) but failed to stain  CD43 transfectants (right). L11 stained CD43 transfectants (left), but not  MAdCAM-1 transfectants (not shown).
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Figure 5: L11 antigen is CD43. L11 (left), but not control mAb (right), stained CD43-transfected CHO-P cells. CHO-P cells were transfected with mouse CD43 or mouse MAdCAM-1 cDNA and stained with L11 mAb or control mAb MECA367 (anti–mouse MAdCAM-1). MECA367 recognized MAdCAM-1 transfectants (not shown) but failed to stain CD43 transfectants (right). L11 stained CD43 transfectants (left), but not MAdCAM-1 transfectants (not shown).

Mentions: Immunofluorescence flow cytometry reveals that L11 antigen is highly expressed by bone marrow neutrophils as well as T cells (not shown). This expression pattern is similar to that of CD43 (10). In addition, the relative molecular mass of the L11 antigen, 100 kD in Western blots (not shown), is also similar to that reported for mouse CD43 (11). Therefore, we next assessed reactivity of L11 with CHO-P cell transfectants expressing mouse CD43 (11). L11 (Fig. 5, left) but not control mAb (Fig. 5, right), stained CD43-transfected CHO-P cells, as did antiCD43 mAb S7 (not shown). L11 failed to stain mocktransfected CHO-P cells or CHO-P cells expressing the irrelevant antigen MAdCAM-1. Thus, L11 can recognize CD43.


Anti-CD43 inhibition of T cell homing.

McEvoy LM, Sun H, Frelinger JG, Butcher EC - J. Exp. Med. (1997)

L11 antigen is CD43. L11 (left), but not control mAb (right),  stained CD43-transfected CHO-P cells. CHO-P cells were transfected  with mouse CD43 or mouse MAdCAM-1 cDNA and stained with L11  mAb or control mAb MECA367 (anti–mouse MAdCAM-1). MECA367  recognized MAdCAM-1 transfectants (not shown) but failed to stain  CD43 transfectants (right). L11 stained CD43 transfectants (left), but not  MAdCAM-1 transfectants (not shown).
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Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2196282&req=5

Figure 5: L11 antigen is CD43. L11 (left), but not control mAb (right), stained CD43-transfected CHO-P cells. CHO-P cells were transfected with mouse CD43 or mouse MAdCAM-1 cDNA and stained with L11 mAb or control mAb MECA367 (anti–mouse MAdCAM-1). MECA367 recognized MAdCAM-1 transfectants (not shown) but failed to stain CD43 transfectants (right). L11 stained CD43 transfectants (left), but not MAdCAM-1 transfectants (not shown).
Mentions: Immunofluorescence flow cytometry reveals that L11 antigen is highly expressed by bone marrow neutrophils as well as T cells (not shown). This expression pattern is similar to that of CD43 (10). In addition, the relative molecular mass of the L11 antigen, 100 kD in Western blots (not shown), is also similar to that reported for mouse CD43 (11). Therefore, we next assessed reactivity of L11 with CHO-P cell transfectants expressing mouse CD43 (11). L11 (Fig. 5, left) but not control mAb (Fig. 5, right), stained CD43-transfected CHO-P cells, as did antiCD43 mAb S7 (not shown). L11 failed to stain mocktransfected CHO-P cells or CHO-P cells expressing the irrelevant antigen MAdCAM-1. Thus, L11 can recognize CD43.

Bottom Line: We selected antilymphocyte monoclonal antibodies (mAbs) for inhibition of lymphocyte binding in vitro to lymph node high endothelial venules (HEV), specialized vessels that support lymphocyte recruitment into lymph nodes. mAb L11 blocks T cell binding to lymph node and Peyer's patch HEV and inhibits T cell extravasation from the blood into organized secondary lymphoid tissues.The L11 antigen is CD43, a sialomucin implicated in vitro in regulation of lymphocyte activation, whose expression is often dysregulated in the Wiskott-Aldrich syndrome.CD43 represents a novel target for experimental and therapeutic manipulation of lymphocyte traffic and may help regulate T cell distribution in vivo.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology, Stanford University, California 94305, USA.

ABSTRACT
The homing of lymphocytes from the blood is controlled by specialized processes of lymphocyte-endothelial cell interaction. Interference with these processes offers the potential to manipulate lymphocyte traffic, and thus to modulate normal and pathologic immune and inflammatory responses. We selected antilymphocyte monoclonal antibodies (mAbs) for inhibition of lymphocyte binding in vitro to lymph node high endothelial venules (HEV), specialized vessels that support lymphocyte recruitment into lymph nodes. mAb L11 blocks T cell binding to lymph node and Peyer's patch HEV and inhibits T cell extravasation from the blood into organized secondary lymphoid tissues. In contrast, L11 has no effect on lymphocyte binding to purified vascular ligands for L-selectin, alpha4beta7, or LFA-1, suggesting that it inhibits by a novel mechanism. The L11 antigen is CD43, a sialomucin implicated in vitro in regulation of lymphocyte activation, whose expression is often dysregulated in the Wiskott-Aldrich syndrome. CD43 represents a novel target for experimental and therapeutic manipulation of lymphocyte traffic and may help regulate T cell distribution in vivo.

Show MeSH
Related in: MedlinePlus