BTLA (C272) expression on CD4+ T cells in Behçet patients
To investigate the peripheral blood levels of B and T lymphocyte attenuator (BTLA/CD272) on T cells and its role in Behçet disease (BD), and to define the role of inhibitory receptors on BD. Materials and methods: Included in this study were 25 patients with BD and 20 healthy control subjects, matched for age and sex. Results: CD4+CD272+ (P < 0.001) and CD3+CD272+ (P < 0.001) T cell levels were significantly higher in BD patients (active and remission) compared to the healthy controls. However, there was no difference between the active patients and those in remission in terms of CD4+CD272+ T cells, while CD3+CD272+ T cell levels were significantly higher in active-phase BD patients compared to patients in the remission phase (P < 0.05). Conclusion: Further functional studies could be implemented to investigate the effectiveness of the present research parameter in the diagnosis or follow-up of certain diseases similar to BD and with obscure etiology, as well as its contribution to immune dysregulation of BD. BTLA can additionally modulate T cell response in BD on different inflammatory areas and it can be upregulated in BD because of T cell activation. The results of the present study indicate that BTLA expression on CD4+ Th (T helper) cells might play a limiting role on the inflammation at peripheral sites or organs in BD.
BTLA (C272) expression on CD4+ T cells in Behçet patients
To investigate the peripheral blood levels of B and T lymphocyte attenuator (BTLA/CD272) on T cells and its role in Behçet disease (BD), and to define the role of inhibitory receptors on BD. Materials and methods: Included in this study were 25 patients with BD and 20 healthy control subjects, matched for age and sex. Results: CD4+CD272+ (P < 0.001) and CD3+CD272+ (P < 0.001) T cell levels were significantly higher in BD patients (active and remission) compared to the healthy controls. However, there was no difference between the active patients and those in remission in terms of CD4+CD272+ T cells, while CD3+CD272+ T cell levels were significantly higher in active-phase BD patients compared to patients in the remission phase (P < 0.05). Conclusion: Further functional studies could be implemented to investigate the effectiveness of the present research parameter in the diagnosis or follow-up of certain diseases similar to BD and with obscure etiology, as well as its contribution to immune dysregulation of BD. BTLA can additionally modulate T cell response in BD on different inflammatory areas and it can be upregulated in BD because of T cell activation. The results of the present study indicate that BTLA expression on CD4+ Th (T helper) cells might play a limiting role on the inflammation at peripheral sites or organs in BD.
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- 1. Saito T, Yamasaki S. Negative feedback of T cell activation through inhibitory adapters and costimulatory receptors. Immunol Rev 2003; 192: 143-60.
- 2. Watanabe N, Gavrieli M, Sedy JR, Yang J, Fallarino F, Loft in SK et al. BTLA is a lymphocyte inhibitory receptor with similarities to CTLA-4 and PD-1. Nat Immunol 2003; 4: 670- 79.
- 3. Sedy JR, Gavrieli M, Potter KG, Hurchla MA, Lindsley RC, Hilder K et al. B and T lymphocyte attenuator regulates T cell activation through interaction with herpes virus entry mediator. Nat Immunol 2005; 6: 90-8.
- 4. Chang YH, Hsieh SL, Chao Y, Chou YC, Lin WW. Proinfl ammatory eff ects of LIGHT through HVEM and LTßR interactions in cultured human umbilical vein endothelial cells. J Biomed Sci 2005; 12: 363-75.
- 5. Croft M. Th e evolving cross talk between co-stimulatory and co-inhibitory receptors: HVEM-BTLA. Trends Immunol 2005; 26: 292-4.
- 6. Hurchla MA, Sedy JR, Gavrieli M, Drake CG, Murphy TL, Murphy KM. B and T lymphocyte attenuator exhibits structural and expression polymorphisms and is highly induced in anergic CD4+ T cells. J Immunol 2005; 174: 3377-85.
- 7. Krieg C, Han P, Stone R, Goularte OD, Kaye J. Functional analysis of B and T lymphocyte attenuator engagement on CD4+ and CD8+ T cells. J Immunol 2005; 175: 6420-7.
- 8. Owada T, Watanabe N, Oki M, Oya Y, Saito Y, Saito T et al. Activation-induced accumulation of B and T lymphocyte attenuator at the immunological synapse in CD4+ T cells. J Leukoc Biol 2010; 87: 425-32.
- 9. Deppong C, Juehne TI, Hurchla M, Friend LD, Shah DD, Rose CM et al. B and T lymphocyte attenuator and programmed death receptor-1 inhibitory receptors are required for termination of acute allergic airway infl ammation. J Immunol 2006; 176: 3909-13.
- 10. Steinberg MW, Turovskaya O, Shaikh RB, Kim G, McCole DF, Pfeff er KA et al. Crucial role for HVEM and BTLA in preventing intestinal infl ammation. J Exp Med 2008; 205: 1463-76.
- 11. Oya Y, Watanabe N, Owada T, Oki M, Hirose K, Suto A et al. Development of autoimmune hepatitis-like disease and production of autoantibodies to nuclear antigens in mice lacking B and T lymphocyte attenuator. Arthritis Rheum 2008; 58: 2498-510.
- 12. Hegele RG. Th e pathology of asthma: brief review. Immunopharmacology 2000; 48: 257-62. 13. Greenwald RJ, Latchman YE, Sharpe AH. Negative coreceptors on lymphocytes. Curr Opin Immunol 2002; 14: 391- 6.
- 14. Deppong C,Degnan JM, Murphy TL,Murphy KM, Green JM. B and T lymphocyte attenuator, BTLA, regulates T cell survival in the lung.J Immunol 2008; 181: 2973-9.
- 15. Liu X, Alexiou M, Martin-Orozco N, Chung Y, Nurieva RI, Ma L et al. A critical role of B and T lymphocyte attenuator in peripheral T cell tolerance induction. J Immunol 2009: 15; 182: 4516-20.