LILRA2 activation inhibits dendritic cell differentiation and antigen presentation to T cells. Journal Article uri icon



  • The differentiation of monocytes into dendritic cells (DC) is a key mechanism by which the innate immune system instructs the adaptive T cell response. In this study, we investigated whether leukocyte Ig-like receptor A2 (LILRA2) regulates DC differentiation by using leprosy as a model. LILRA2 protein expression was increased in the lesions of the progressive, lepromatous form vs the self-limited, tuberculoid form of leprosy. Double immunolabeling revealed LILRA2 expression on CD14+, CD68+ monocytes/macrophages. Activation of LILRA2 on peripheral blood monocytes impaired GM-CSF induced differentiation into immature DC, as evidenced by reduced expression of DC markers (MHC class II, CD1b, CD40, and CD206), but not macrophage markers (CD209 and CD14). Furthermore, LILRA2 activation abrogated Ag presentation to both CD1b- and MHC class II-restricted, Mycobacterium leprae-reactive T cells derived from leprosy patients, while cytokine profiles of LILRA2-activated monocytes demonstrated an increase in TNF-alpha, IL-6, IL-8, IL-12, and IL-10, but little effect on TGF-beta. Therefore, LILRA2 activation, by altering GM-CSF-induced monocyte differentiation into immature DC, provides a mechanism for down-regulating the ability of the innate immune system to activate the adaptive T cell response while promoting an inflammatory response.

publication date

  • December 15, 2007

has subject area

has restriction

  • bronze

Date in CU Experts

  • November 15, 2013 1:51 AM

Full Author List

  • Lee DJ; Sieling PA; Ochoa MT; Krutzik SR; Guo B; Hernandez M; Rea TH; Cheng G; Colonna M; Modlin RL

author count

  • 10

Other Profiles

International Standard Serial Number (ISSN)

  • 0022-1767

Additional Document Info

start page

  • 8128

end page

  • 8136


  • 179


  • 12