It is feasible that, in SLE patients, defects on these receptors highlight ILT2 and ILT4 function; however, even when the function of ILT4 is preserved in DC from SLE patients, the diminished percentages of ILT4 circulating DC may have a role in SLE pathogenesis. This evidence concerns the gene LILRB2 and systemic lupus erythematosus.