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Rev. Bras. Reumatol. vol.52 número1 en v52n1a01

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EDITORIAL

1 Rev Bras Reumatol 2012;52(1):1-2

T

he HLA-G gene has several peculiarities that dis-tinguish it from the class I HLA genes. Its singular molecular structure provides a limited antigen presen-tation and allows the modulation of immune system cells (NK and lymphomononuclear cells), and the result is that HLA-G acts like a tolerogenic and immunosuppressive molecule.1

Its major physiological function lies in participating in the tolerance between maternal and fetal cells in the placental interface.2 HLA-G is implicated in the etiopathogenesis of

several human diseases, such as chronic viral infections (HIV, cytomegalovirus, hepatitis C and hepatitis B), rejection to the transplantation of solid organs (kidney, heart), neoplasias, and autoimmune diseases (rheumatoid arthritis, systemic lupus erythematosus, systemic sclerosis, multiple sclerosis, and type I diabetes mellitus).3 In this issue, Brenol CV et al.4

reviewed the role of HLA-G in several autoimmune rheumatic

h

e therapeutic potential of the HLA-G molecule

© 2012 Elsevier Editora Ltda. All rights reserved.

diseases (rheumatoid arthritis, systemic lupus erythematosus, systemic sclerosis, Behçet’s disease, juvenile idiopathic arthritis, Kawasaki disease, infl ammatory myopathies, and sarcoidosis). The authors provide a general panel of the molecular structure of HLA-G, its major functions, and how the study of the polymorphism of its alleles associates with the occurrence of autoimmune rheumatic diseases. Because HLA-G is an immunosuppressive and tolerance-inducing molecule, the possibility of its future use in the treatment of autoimmune diseases, including the rheumatic diseases, has been considered.5

Paulo Louzada-Junior Max Victor Carioca Freitas

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EDITORIAL

2 Rev Bras Reumatol 2012;52(1):1-2

REFERENCES

REFERÊNCIAS

1. Donadi EA, Castelli EC, Arnaiz-Villena A, Roger M, Rey D, Moreau P. Implications of the polymorphism of HLA-G on its function, regulation, evolution and disease association. Cell Mol Life Sci 2011; 68(3):369–95.

2. Yao YQ, Barlow DH, Sargent IL. Differential expression of alternatively spliced transcripts of HLA-G in human preimplantation embryos and inner cell masses. J Immunol 2005; 175(12):8379–85. 3. Carosella ED, Moreau P, Lemaoult J, Rouas-Freiss N. HLA-G: from biology to clinical beneits. Trends Immunol 2008; 29(3):125–32. 4. Brenol CV, Veit TD, Chies JA, Xavier RM. The role of the HLA-G

gene and molecule on the clinical expression of rheumatologic diseases. Rev Bras Reumatol 2012; 52(1):75–91.

Referências

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