It is tempting to speculate therefore that increased SIGLEC1 expression and/or the numbers of circulating Siglec-1+ monocyte/macrophages in UA and RA may reflect a homeostatic feedback mechanism engaged to limit increased Treg numbers and/or to regulate the Treg: Teff balance at a critical point in the progression from acute to chronic inflammatory disease status. Here, SIGLEC1 is linked to rheumatoid arthritis.