Our discovery identifies the events downstream of the Fabp5/calnexin C-tail domain complex formation at the cytosol/ER membrane interface, culminating with the increased production of sCD200, as well as CD200 itself, as novel avenues for the development of new therapeutic strategies to minimize the invasion of the CNS with potentially disease-inducing T-cells, such as in MS. Here, CD200 is linked to myeloid sarcoma.