Altered immunoregulation in rheumatoid arthritis: the role of regulatory T cells and proinflammatory Th17 cells and therapeutic implications.
In recent years several studies investigated the role of T lymphocyte subpopulations in the pathogenesis of rheumatoid arthritis (RA). Pathogenic Th17 cells mediate pannus growth, osteoclastogenesis, and synovial neoangiogenesis; hence they are key players in the development of the disease. On the other hand, regulatory T (Treg) cells are a T cell subset whose peculiar function is to suppress autoreactive lymphocytes. The imbalance between Th17 and Treg cells has been identified as a crucial event in the pathogenesis of RA. In addition, the effects of currently employed RA therapeutic strategies on these lymphocyte subpopulations have been extensively investigated. This review article aims to discuss current knowledge on Treg and Th17 cells in RA and possible implications of their therapeutic targeting in this disorder.
Rheumatology Unit, Department of Medicine, University of Perugia, 06132 Perugia, Italy.
Alessia
A
Alunno
Department of Experimental and Clinical Medicine, Section of Anatomy and Histology, University of Florence, 50134 Florence, Italy.
Mirko
0000-0003-3956-8480
M
Manetti
Rheumatology Unit, Department of Medicine, University of Perugia, 06132 Perugia, Italy.
Sara
S
Caterbi
Department of Experimental and Clinical Medicine, Section of Anatomy and Histology, University of Florence, 50134 Florence, Italy.
Lidia
L
Ibba-Manneschi
Rheumatology Unit, Department of Medicine, University of Perugia, 06132 Perugia, Italy.
Onelia
O
Bistoni
Rheumatology Unit, Department of Medicine, University of Perugia, 06132 Perugia, Italy.
Elena
E
Bartoloni
Rheumatology Unit, Department of Medicine, University of Perugia, 06132 Perugia, Italy.
Valentina
V
Valentini
Rheumatology Unit, Department of Medicine, University of Perugia, 06132 Perugia, Italy.
Riccardo
R
Terenzi
Rheumatology Unit, Department of Medicine, University of Perugia, 06132 Perugia, Italy.
Roberto
R
Gerli
D000069594:Abatacept / Q000627:therapeutic use; D000305:Adrenal Cortex Hormones / Q000627:therapeutic use; D000818:Animals; D061067:Antibodies, Monoclonal, Humanized / Q000627:therapeutic use; D018501:Antirheumatic Agents / Q000627:therapeutic use; D001172:Arthritis, Rheumatoid / Q000097:blood* / Q000628:therapy*; D044127:Epigenesis, Genetic; D006801:Humans; D007249:Inflammation / Q000276:immunology; D008214:Lymphocytes / Q000166:cytology; D051379:Mice; D013583:Synovial Membrane / Q000378:metabolism; D050378:T-Lymphocytes, Regulatory / Q000166:cytology* / Q000276:immunology; D058504:Th17 Cells / Q000166:cytology*; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors
D000305:Adrenal Cortex Hormones; D061067:Antibodies, Monoclonal, Humanized; D018501:Antirheumatic Agents; D014409:Tumor Necrosis Factor-alpha; D000069594:Abatacept; C502936:tocilizumab