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. The gene discussed is LILRB1; the disease is systemic lupus erythematosus.