Redundant and alternative roles for activating Fc receptors and complement in an antibody-dependent model of autoimmune vitiligo

Immunity. 2002 Jun;16(6):861-8. doi: 10.1016/s1074-7613(02)00327-8.


Complement and Fc receptor (FcR)-positive cells mediate effector functions of antibodies. Antibody-dependent immunity against the melanosome membrane glycoprotein gp75/tyrosinase-related protein-1 (TYRP-1) of melanocytes leads to autoimmune hypopigmentation (vitiligo) in mice. Hypopigmentation occurred in mice deficient in activating FcR containing the common gamma subunit (Fc gamma R gamma(-/-)) and in mice deficient in the C3 complement component. Mice doubly deficient in both Fc gamma R gamma and C3 did not develop hypopigmentation, suggesting that complement and Fc gamma R formed redundant mechanisms. Following passive immunization with antibody, no further adaptive immune responses were required. Chimeric Fc gamma R gamma(-/-),C3(-/-) mice reconstituted with bone marrow from either Fc gamma R gamma(-/-) or C3(-/-) mice or adoptively transferred with Fc gamma R gamma(+/-) macrophages did develop antibody-mediated hypopigmentation. Thus, either complement or macrophages expressing activating Fc gamma R can independently and alternatively mediate disease in a model of autoimmune vitiligo.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adoptive Transfer
  • Animals
  • Complement Activation / physiology*
  • Complement C3 / immunology
  • Genotype
  • Immunization, Passive
  • Macrophages / immunology
  • Melanocytes / immunology
  • Membrane Glycoproteins / immunology*
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Oxidoreductases*
  • Receptors, Fc / physiology*
  • Recombinant Fusion Proteins / immunology
  • Vitiligo / immunology*


  • Complement C3
  • Membrane Glycoproteins
  • Receptors, Fc
  • Recombinant Fusion Proteins
  • Oxidoreductases
  • Tyrp1 protein, mouse