I dunno, I think that Trogocytosis sounds like something that trolls do. But actually, it appears that T cells do this, and in particular, T reg cells do it to antigen presenting cells and to other T cells (See Picirillo, Autoimmunity 2011). What is Trogocytosis? It’s the process by which cells acquire bits of membrane (and whatever else is on it) from other nearby cells. Dendritic cells do it to tumors, and it may be critically important for host defense against cancer. Perhaps more to the point for autoimmunity, both Teff and nTregs can acquire MHC filled with peptides from antigen presenting cells (APCs).
Maybe Trogocytosis is how nTreg cell-contact mediated suppression works. Take a look, if you have a minute, at Clare Allen’s  nice review paper on Tregs – apparently the Tregs that are the most effective down-regulators are the ones with MHC class II (HLA DR) on their surface.

Does any one wonder why some Tregs are armed with HLA DR, or where it comes from? Apparently, 20 to 30% of CD4+CD25high Tregs express HLA-DR (See Clare’s previous paper). Do the HLA DR come from APCs, and are they filled with peptides that then become the target of immune suppression (once the T cell that recognizes the antigen docks on the Treg, then the Treg can exert its effect).

I think it makes sense for Tregs to actively acquire MHC plus peptides from neighboring APCS. That way they can present the MHC and cognate epitope to passing T cells, and directly control their response. Too much inflammation going on? Then arm the Tregs with DR and the corresponding epitope, get the T effectors to dock directly on the Treg, and you have a means of shutting of the T cell responders. This off-switch can be precise, local, and antigen-specific.

Now if we can only capture that concept and turn it into a treatment for autoimmune disease. Perhaps we can use Trogocytosis to turn autoreactive T cells into stone.