Involvement of T-Lymphocytes in Periodontal Disease and in Direct and Indirect Induction of Bone Resorption
Tóm tắt
Periodontal disease is a peripheral infection involving species of Gram-negative organisms. T-lymphocytes can be found in the dense inflammatory infiltrate in this disease. CD4+ and CD8+ T-cells are present in periodontal lesions, as are memory/activated T-lymphocytes. In addition, Th1- and Th2-type T-lymphocytes and their associated cytokines with a subtle polarization to Th 1 may be present. Th1-type T-cells up-regulate the production of pro-inflammatory cytokines IL-1 and TNF-α, which can induce bone resorption indirectly by promoting differentiation of osteoclast precursors and subsequently by activating osteoclasts. Such osteoclast differentiation is dependent on stimulation of osteoprotegerin ligand (OPG-L) production by osteoblastic cells. By contrast, activated T-cells, by virtue of direct production and expression of OPG-L, can directly promote osteoclast differentiation. OPG-L appears to be predominantly expressed on Th1-type cells. The direct and indirect T-cell involvement in periodontal bone resorption appears to be dependent on the degree of Th 1-type T-cell recruitment into inflamed gingival tissues. This T-cell recruitment is regulated by adhesion molecules and chemokines/chemokine receptors. The adhesion molecules involved include a4 and a6 integrins, LFA-1, and ICAM-1. The Th1-type T-cells preferentially express CCR5 and CXCR3, which are found prominently in diseased gingivae. By contrast, little CCR4, expressed by Th2-type T-cells, can be detected. Also, the chemokine ligands RANTES, MIP1-α (both CCR5), and IP-10 (CXCR3 ligand) were elevated in inflamed periodontal tissues. The T-cell features in diseased periodontal tissues can be compared with those in rheumatoid arthritis, wherein bone resorption often attributed to Th1-type T-cell involvement has also been demonstrated.
Từ khóa
Tài liệu tham khảo
Arenzana-Seisdedos F., Virelizier JL, Fiers W. (1985). Interferons as macrophage-activating factors. III. Preferential effects of interferon-gamma on the interleukin I secretory potential of fresh or aged human monocytes. J Immunol 134:2444-2448.
Assuma R., Oates T., Cochran D., Amar S., Graves DT (1998). IL-1 and TNF antagonists inhibit the inflammatory response and bone loss in experimental periodontitis. J Immunol 160:403-409.
Crawford JM (1991). Distribution of ICAM-1, LFA-3 and HLA-DR in healthy and diseased gingival tissues. J Periodont Res 27:291-298.
de Waal Malefyt R., Yssel H., de Vries JE (1993). Direct effects of IL-10 on subsets of human CD4+ T cell cloning and resting T cells; specific inhibition of IL-2 production and proliferation. I Immunol 150:4754-4765.
Ebersole JL, Taubman MA, Smith DJ, Hammond BF, Frey DE ( 1982). Human immune responses to oral microorganisms. I. Association of localized juvenile periodontitis (LJP) with serum antibody responses to Actinobacillus actinomycetemcomitans. Clin Exp Immunol 47:43-52.
Ebersole JL, Cappelli D., Steffen MJ (2000). Antigenic specificity of gingival crevicular fluid antibody to Actinobacillus actinomycetemcomitans. J Dent Res 74:1362-1370.
Esch T., Taubman MA (1997). Cytokine profiles of gingival mononuclear cells measured by intracellular fluorescent staining (abstract). J Dent Res 76:231.
Fujihashi K., Yamamoto M., Hiroi T., Bamberg TV, McGhee JR, Kiyono H. (1996). Selected Th I and Th2 cytokine mRNA expression by CD4+ T cells isolated from human gingival tissues. Clin Exp Immunol 103:422-428.
Gainet J., Dang PMC, Chollet-Martin S., Brion M., Sixou M., Hakim J., et al. (1999). Neutrophil dysfunctions, IL-8, and soluble L-selectin plasma levels in rapidly progressive versus adult and localized juvenile periodontitis: variation according to disease severity and microbial flora. J Immunol 163:5013-5019.
Gazzinelli RT, Wysocka M., Hieny S., Scharton-Kersten T., Cheever A., Kuhn T., et al. (1996). In the absence of endogenous 1L-10, mice acutely infected with Toxoplasma gondii succumb to a lethal immune response dependent on CD4+ T cells and accompanied by overproduction of IL-12, IFN-gamma and TNF-alpha. J Immunol 157:798-805.
Ho GJ (1992). Bacterial arthritis. Curr Opin Rheumatol 4:509-515.
Hosokawa Y., Kawai T., Shimizu H., Yamaguchi D., Nakanishi T., Taubman MA, et al. (2001). Increased CCR5+ and CXCR3+ T cell and RANTES, MIP-1α and IP-10 expression in inflamed periodontal tissue indicate selective T cell recruitment. Submitted.
Hunter CA, Ellis-Neyes LA, Slifer T., Kanaly S., Grunig G., Fort M., et al. (1997). IL-10 is required to prevent immune hyperactivity during infection with Trypanosoma cruzi. J Immunol 158:3311-3316.
Ianeway CAJ (1998). The road less traveled by: the role of innate immunity in the adaptive immune response. J Immunol 161:539-544.
Iosien R., Wong RB, Li H., Steinman RM, Choi Y. ( 1999). TRANCE, a TNF family member, is differentially expressed on T cell subsets and induces cytokine production in dendritic cells. J Immunol 162:2562-2568.
Kawai T., Seki M., Hiromatsu K., Eastcott JW, Watts GFM, Sugai M., et al. (1999). Selective diapedesis of Th1 cells induced by endothelial cell RANTES. J Immunol 163:3269-3278.
Loetscher P., Uguccioni M., Bordoli L., Baggiolini L., Moser B. (1998). CCR5 is characteristic of Th1 lymphocytes. Nature 391:344-345.
Lundqvist C., Hammarstrom M-L. (1993). T-cell receptor γδ-expressing intraepithelial lymphocytes are present in normal and chronically inflamed human gingiva. Immunology 79:38-45.
Lundqvist C., Baranov V., Teglund S., Hammarstrom S., Hammarstrom M-L. (1994). Cytokine profile and ultrastructure of intraepithelial γδ T cells in chronically inflamed human gingiva suggest a cytotoxic effector function. J Immunol 153:2302-2311.
Macatonia SE, Hosken NA, Litton M., Vieira P., Hsieh C.S, Culpepper JA, et al. (1995). Dendritic cells produce IL-12 and direct the development of Th 1 cells from naïve CD4+ T cells. J Immunol 154:5071-5079.
Mosmann TR, Cherwinski H., Bond MW, Giedlin MA, Coffman R. (1986). Two types of murine helper T cell clone. I. Definition according to profiles of lymphokine activities and secreted proteins. J Immunol 136:2348-2357.
Murakami S., Saho T., Shimabukuro Y., Isoda R., Miki Y., Okada H. (1993). Very late antigen integrins are involved in the adhesive interaction of lymphoid cells to human gingival fibroblasts. Immunology 79:425-433.
Onoe Y., Miyaura C., Kaminakayashiki T., Nagai Y., Noguchi K., Chen Q-R., et al. (1996). IL-13 and IL-4 inhibit bone resorption by suppressing cyclooxygenase-2-dependent prostaglandin synthesis in osteoblasts. J Immunol 156:758-764.
Page RC, Schroeder HA (1976). Pathogenesis of inflammatory periodontal disease. A summary of current work. Lab Invest 34:235-249.
Pascalis L., Aresu G., Pia G. (1999). Long-term efficacy and toxicity of cyclosporin A + fluocortolone + methotrexate in the treatment of rheumatoid arthritis. J Rheumatol 17:679-688.
Pfeilschifter J., Chenu C., Bird A., Mundy GR, Roodman GD (1989). Interleukin-1 and tumor necrosis factor stimulate the formation of human osteoclast-like cells in vitro. J Bone Min Res 4:113-118.
Snyderman R., McCarty GA (1982). Analogous mechanisms of tissue destruction in rheumatoid arthritis and periodontal disease. In: Host-parasite interaction in periodontal diseases. Genco R, Mergenhagen S, editors. Washington, DC: ASM Press, pp. 354-361.
Socransky SS, Haffajee AD, Ximenez-Fyvie LA, Feres M., Mager D. (2000). Ecological considerations in the treatment of Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis periodontal infections. Periodontology 2000 20:341-362.
Taubman MA, Eastcott JW, Shimauchi H., Takeichi O., Smith DJ (1994). Modulatory role of T lymphocytes in periodontal inflammation. In: Molecular pathogenesis of periodontal disease. Genco R, Hamada S, Lehner T, McGhee JR, Mergenhagen SE, editors. Washington, DC: ASM Press, pp. 147-157.
Thomas R., Quinn C. (1996). Functional differentiation of dendritic cells in rheumatoid arthritis: role of CD86 in the synovium. J Immunol 156:3074-3086.
Verhasselt V., Bueclens C., Willems F., De Groote D., Haeffner-Cavallion N., Goldman M. (1997). Bacterial lipopolysaccharide stimulates the production of cytokines and the expression of costimulatory molecules by human peripheral blood dendritic cells: evidence for a soluble CD14-dependent pathway. J Immunol 158:2919-2925.
Yamamoto N., Sakai F., Yamazaki H., Kawai Y., Nakahara K., Okuhara M. (1996). Effect of FR133605, a novel cytokine suppressive agent, on bone and cartilage destruction in adjuvant arthritic rats. J Rheumatol 23:1778-1783.
Yun TJ, Chaudhary PM, Shu GL, Frazer JK, Ewings MK, Schwartz SM, et al. (1998). OPG/FDCR-1, a TNF receptor family member, is expressed in lymphoid cells and is up-regulated by ligating CD40. J Immunol 161:6113-6121.
Zissel G., Schlaak M., Muller-Quernheim I. (1996). Regulation of cytokine release by alveolar macrophages treated with interleukin-4, interleukin-10, or transforming growth factor beta. Eur Cytokine Netw 7:59-66.