Anti- Concanavalin

For identification the lectins must be labeled. The best labels are biotin (streptavidin-enzyme conjugate) or digoxigenin (anti-digoxigenin antibody-enzyme conjugate), but in the case of Concanavalin A, direct labeling with HRP is possible (see below). 

Figure 2. Inhibition by lectins of the binding of, 2>I F(ab) fragments of anti-H-2.4 IgG to lymphocytes. (A) M. pomifera agglutinin (Q) concanavalin A (Q) W. floribunda mitogen (O) S. japonica agglutinin.

Lymphotoxicity (cytotoxicity or functional impairment, e.g., proliferation upon anti-CD3 or anti-CD28 stimulation) [7] Human peripheral blood lymphocytes (whole blood or PBMC) or rodent splenocytes are typically used. Polyclonal stimuli include anti-CD3, anti-CD28, plant lectins such as concanavalin A (ConA) and phytohemagglutinin (PHA), superantigens etc. Mixed lymphocyte reactions possible but less used for immunotoxicity... 

Nakano Y, Pross SH, Friedman H (1992) Modulation of interleukin 2 activity by delta-9-tetrahydrocannabinol after stimulation with concanavalin A, phytohemagglutinin, or anti-CD3 antibody. Proc Soc Exp Biol Med 201 165-168... 

Traces of concanavalin A have been detected in samples of purified aj-anti-trypsin after affinity chromatography on immobilized concanavalin A. The interfering lectin may be removed by adsorption of the Oj-antitrypsin on thiol-activated macroporous agarose. 

Both lymphotactin and fractalkine are expressed in an activation-dependent manner. The expression of lymphotactin is upregulated by phorbol ester and concanavalin 1 in T-cells isolated from peripheral blood (Middel et al., 2001). It can be inhibited by anti-inflammatory steroid dexamethasone or immunosuppressive drugs such as cyclosporine A and FK506 (Middel et al., 2001). These agents also regulate the expression of lymphotactin receptor XCRl on T-cells in a manner similar to the regulation of lymphotactin expression. The nuclear factor of activated T-cells (NF-AT) family s transcription factors are likely to be involved in the activation-induced expression and cyclosporine A-dependent inhibition of lymphotactin (Yoshida et al., 1999). 

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