Wikipedia tells us The protein encoded by this gene is a type-1 membrane glycoprotein, which contains two immunoglobulin domains, and thus belongs to the immunoglobulin superfamily. Studies of the related genes in mouse and rat suggest that this gene may regulate myeloid cell activity and delivers an inhibitory signal for the macrophage lineage in diverse tissues.
So why should this be of any interest to a CLL doctor? A paper just published on line in Leukemia Research gives the answer. CD200 turns out to be overexpressed on CLL cells. Why is it there? It is thought that prolonged B cell receptor stimulation activates the MEK/ERK pathway and that up-regulation of ERK causes the upregulation of surface CD200. What is it doing there? It has three apparent functions. First it inhibits T cell proliferation. Second it suppresses T cells specific for a tumor associated angigen. Third it enhances regulatory T cells.
Why does this matter? There is some evidence that a patient's own T cells can be induced to kill his or her own CLL cells, but that this effect is inhibited by CD200. It is conceivable therefore that blockade of CD200 with an antibody would enhance the body's ability to rid itself of the tumor.