Advances in understanding the pathogenesis of primary Sjögren's syndrome
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Alamanos, Y. et al. Epidemiology of primary Sjogren's syndrome in north-west Greece, 1982–2003. Rheumatology (Oxford) 45, 187–191 (2006).
Bowman, S. J., Ibrahim, G. H., Holmes, G., Hamburger, J. & Ainsworth, J. R. Estimating the prevalence among Caucasian women of primary Sjogren's syndrome in two general practices in Birmingham, UK. Scand. J. Rheumatol. 33, 39–43 (2004).
Tomsic, M., Logar, D., Grmek, M., Perkovic, T. & Kveder, T. Prevalence of Sjögren's syndrome in Slovenia. Rheumatology (Oxford) 38, 164–170 (1999).
Delaleu, N., Nguyen, C. Q., Peck, A. B. & Jonsson, R. Sjögren's syndrome: studying the disease in mice. Arthritis Res. Ther. 13, 217 (2011).
Mariette, X. & Gottenberg, J. E. Pathogenesis of Sjögren's syndrome and therapeutic consequences. Curr. Opin. Rheumatol. 22, 471–477 (2010).
Bave, U. et al. Activation of the type I interferon system in primary Sjögren's syndrome: a possible etiopathogenic mechanism. Arthritis Rheum. 52, 1185–1195 (2005).
Kang, K. Y. et al. Impact of interleukin-21 in the pathogenesis of primary Sjögren's syndrome: increased serum levels of interleukin-21 and its expression in the labial salivary glands. Arthritis Res. Ther. 13, R179 (2011).
Ittah, M. et al. Viruses induce high expression of BAFF by salivary gland epithelial cells through TLR- and type-I IFN-dependent and -independent pathways. Eur. J. Immunol. 38, 1058–1064 (2008).
Miceli-Richard, C. et al. Association of an IRF5 gene functional polymorphism with Sjögren's syndrome. Arthritis Rheum. 56, 3989–3994 (2007).
Miceli-Richard, C. et al. The CGGGG insertion/deletion polymorphism of the IRF5 promoter is a strong risk factor for primary Sjögren's syndrome. Arthritis Rheum. 60, 1991–1997 (2009).
Nordmark, G. et al. Additive effects of the major risk alleles of IRF5 and STAT4 in primary Sjögren's syndrome. Genes Immun. 10, 68–76 (2009).
Gestermann, N. et al. STAT4 is a confirmed genetic risk factor for Sjögren's syndrome and could be involved in type 1 interferon pathway signaling. Genes Immun. 11, 432–438 (2010).
Korman, B. D. et al. Variant form of STAT4 is associated with primary Sjögren's syndrome. Genes Immun. 9, 267–270 (2008).
Lessard, C. J. et al. Identification of multiple Sjögren's syndrome susceptibility loci [abstract OP0020]. Ann.Rheum. Dis. 72 (Suppl. 3), 54 (2013).
Alevizos, I., Alexander, S., Turner, R. J. & Illei, G. G. MicroRNA expression profiles as biomarkers of minor salivary gland inflammation and dysfunction in Sjögren's syndrome. Arthritis Rheum. 63, 535–544 (2011).
Hooks, J. J. et al. Immune interferon in the circulation of patients with autoimmune disease. N. Engl. J. Med. 301, 5–8 (1979).
Gottenberg, J. E. et al. Activation of IFN pathways and plasmacytoid dendritic cell recruitment in target organs of primary Sjögren's syndrome. Proc. Natl Acad. Sci. USA 103, 2770–2775 (2006).
Hjelmervik, T. O., Petersen, K., Jonassen, I., Jonsson, R. & Bolstad, A. I. Gene expression profiling of minor salivary glands clearly distinguishes primary Sjögren's syndrome patients from healthy control subjects. Arthritis Rheum. 52, 1534–1544 (2005).
Emamian, E. S. et al. Peripheral blood gene expression profiling in Sjögren's syndrome. Genes Immun. 10, 285–296 (2009).
Iwakiri, D. et al. Epstein–Barr virus (EBV)-encoded small RNA is released from EBV-infected cells and activates signaling from Toll-like receptor 3. J. Exp. Med. 206, 2091–2099 (2009).
Deshmukh, U. S., Nandula, S. R., Thimmalapura, P. R., Scindia, Y. M. & Bagavant, H. Activation of innate immune responses through Toll-like receptor 3 causes a rapid loss of salivary gland function. J. Oral Pathol. Med. 38, 42–47 (2009).
Zheng, L., Zhang, Z., Yu, C. & Yang, C. Expression of Toll-like receptors 7, 8, and 9 in primary Sjögren's syndrome. Oral Surg. Oral Med. Oral Pathol. Oral Radiol. Endod. 109, 844–850 (2010).
Nandula, S. R., Scindia, Y. M., Dey, P., Bagavant, H. & Deshmukh, U. S. Activation of innate immunity accelerates sialoadenitis in a mouse model for Sjögren's syndrome-like disease. Oral Dis. 17, 801–807 (2011).
Yamano, S. et al. Retrovirus in salivary glands from patients with Sjögren's syndrome. J. Clin. Pathol. 50, 223–230 (1997).
Gottenberg, J. E. Primary Sjögren's syndrome: pathophysiological, clinical and therapeutic advances. Joint Bone Spine 76, 591–594 (2009).
Fleck, M., Kern, E. R., Zhou, T., Lang, B. & Mountz, J. D. Murine cytomegalovirus induces a Sjögren's syndrome-like disease in C57Bl/6-lpr/lpr mice. Arthritis Rheum. 41, 2175–2184 (1998).
Sisto, M. et al. A failure of TNFAIP3 negative regulation maintains sustained NF-κB activation in Sjögren's syndrome. Histochem. Cell Biol. 135, 615–625 (2011).
Peng, B. et al. Defective feedback regulation of NF-κB underlies Sjögren's syndrome in mice with mutated κB enhancers of the IκBα promoter. Proc. Natl Acad. Sci. USA 107, 15193–15198 (2010).
Mackay, F. et al. Mice transgenic for BAFF develop lymphocytic disorders along with autoimmune manifestations. J. Exp. Med. 190, 1697–1710 (1999).
Batten, M. et al. TNF deficiency fails to protect BAFF transgenic mice against autoimmunity and reveals a predisposition to B cell lymphoma. J. Immunol. 172, 812–822 (2004).
Mariette, X. et al. The level of BLyS (BAFF) correlates with the titre of autoantibodies in human Sjögren's syndrome. Ann. Rheum. Dis. 62, 168–171 (2003).
Daridon, C. et al. Aberrant expression of BAFF by B lymphocytes infiltrating the salivary glands of patients with primary Sjögren's syndrome. Arthritis Rheum. 56, 1134–1144 (2007).
Lavie, F. et al. B-cell activating factor of the tumour necrosis factor family expression in blood monocytes and T cells from patients with primary Sjögren's syndrome. Scand. J. Immunol. 67, 185–192 (2008).
Litinskiy, M. B. et al. DCs induce CD40-independent immunoglobulin class switching through BLyS and APRIL. Nat. Immunol. 3, 822–829 (2002).
Ittah, M. et al. B-cell-activating factor expressions in salivary epithelial cells after dsRNA virus infection depends on RNA-activated protein kinase activation. Eur. J. Immunol. 39, 1271–1279 (2009).
Ittah, M. et al. Induction of B cell-activating factor by viral infection is a general phenomenon, but the types of viruses and mechanisms depend on cell type. J. Innate Immun. 3, 200–207 (2011).
Brkic, Z. et al. Prevalence of interferon type I signature in CD14 monocytes of patients with Sjögren's syndrome and association with disease activity and BAFF gene expression. Ann. Rheum. Dis. 72, 728–735 (2013).
Ambrus, J. L. Jr & Fauci, A. S. Human B lymphoma cell line producing B cell growth factor. J. Clin. Invest. 75, 732–739 (1985).
Shen, L. et al. Development of autoimmunity in IL-14α-transgenic mice. J. Immunol. 177, 5676–5686 (2006).
Shen, L. et al. IL-14 alpha, the nexus for primary Sjögren's disease in mice and humans. Clin. Immunol. 130, 304–312 (2009).
Suresh, L., Ambrus, J. J. & Shen, L. Stages of Sjögren's syndrome defined by immune mediators [abstract 515]. Arthritis Rheum. 64 (Suppl. 10), S225 (2012).
Halse, A., Tengner, P., Wahren-Herlenius, M., Haga, H. & Jonsson, R. Increased frequency of cells secreting interleukin-6 and interleukin-10 in peripheral blood of patients with primary Sjögren's syndrome. Scand. J. Immunol. 49, 533–538 (1999).
Perrier, S. et al. Increased serum levels of interleukin 10 in Sjögren's syndrome; correlation with increased IgG1. J. Rheumatol. 27, 935–939 (2000).
Ogden, C. A. et al. Enhanced apoptotic cell clearance capacity and B cell survival factor production by IL-10-activated macrophages: implications for Burkitt's lymphoma. J. Immunol. 174, 3015–3023 (2005).
Mauri, C. & Blair, P. A. Regulatory B cells in autoimmunity: developments and controversies. Nat. Rev. Rheumatol. 6, 636–643 (2010).
Iwata, Y. et al. Characterization of a rare IL-10-competent B-cell subset in humans that parallels mouse regulatory B10 cells. Blood 117, 530–541 (2011).
Vitali, C. et al. Classification criteria for Sjögren's syndrome: a revised version of the European criteria proposed by the American-European Consensus Group. Ann. Rheum. Dis. 61, 554–558 (2002).
Clancy, R. M. et al. Impaired clearance of apoptotic cardiocytes is linked to anti-SSA/Ro and -SSB/La antibodies in the pathogenesis of congenital heart block. J. Clin. Invest. 116, 2413–2422 (2006).
Tengner, P., Halse, A. K., Haga, H. J., Jonsson, R. & Wahren-Herlenius, M. Detection of anti-Ro/SSA and anti-La/SSB autoantibody-producing cells in salivary glands from patients with Sjögren's syndrome. Arthritis Rheum. 41, 2238–2248 (1998).
Candon, S., Gottenberg, J. E., Bengoufa, D., Chatenoud, L. & Mariette, X. Quantitative assessment of antibodies to ribonucleoproteins in primary Sjögren syndrome: correlation with B-cell biomarkers and disease activity. Ann. Rheum. Dis. 68, 1208–1212 (2009).
Topfer, F., Gordon, T. & McCluskey, J. Intra- and intermolecular spreading of autoimmunity involving the nuclear self-antigens La (SS-B) and Ro (SS-A). Proc. Natl Acad. Sci. USA 92, 875–879 (1995).
Lindop, R. et al. Molecular signature of a public clonotypic autoantibody in primary Sjögren's syndrome: a “forbidden” clone in systemic autoimmunity. Arthritis Rheum. 63, 3477–3486 (2011).
Lindop, R. et al. Long-term humoral autoimmunity to Ro60 in primary Sjögren's syndrome is driven by clonal succession [abstract 2676]. Arthritis Rheum. 64 (Suppl. 10), S1135 (2012).
Amft, N. et al. Ectopic expression of the B cell-attracting chemokine BCA-1 (CXCL13) on endothelial cells and within lymphoid follicles contributes to the establishment of germinal center-like structures in Sjögren's syndrome. Arthritis Rheum. 44, 2633–2641 (2001).
Bombardieri, M. et al. Inducible tertiary lymphoid structures, autoimmunity, and exocrine dysfunction in a novel model of salivary gland inflammation in C57BL/6 mice. J. Immunol. 189, 3767–3776 (2012).
Salomonsson, S. et al. Cellular basis of ectopic germinal center formation and autoantibody production in the target organ of patients with Sjögren's syndrome. Arthritis Rheum. 48, 3187–3201 (2003).
Winter, S. et al. The chemokine receptor CXCR5 is pivotal for ectopic mucosa-associated lymphoid tissue neogenesis in chronic Helicobacter pylori-induced inflammation. J. Mol. Med. (Berl.) 88, 1169–1180 (2010).
Maehara, T. et al. Selective localization of T helper subsets in labial salivary glands from primary Sjögren's syndrome patients. Clin. Exp. Immunol. 169, 89–99 (2012).
Gong, Y. et al. Salivary gland epithelial cells are capable to directly induce the differentiation of IL-21-secreting follicular helper CD4 T cells in primary Sjögren's syndrome [abstract]. Arthritis Rheum. 63 (Suppl. 10), 774 (2011).
Dong, W., Zhu, P., Wang, Y. & Wang, Z. Follicular helper T cells in systemic lupus erythematosus: a potential therapeutic target. Autoimmun. Rev. 10, 299–304 (2011).
Zintzaras, E., Voulgarelis, M. & Moutsopoulos, H. M. The risk of lymphoma development in autoimmune diseases: a meta-analysis. Arch. Intern. Med. 165, 2337–2344 (2005).
Theander, E. et al. Lymphoma and other malignancies in primary Sjögren's syndrome: a cohort study on cancer incidence and lymphoma predictors. Ann. Rheum. Dis. 65, 796–803 (2006).
Smedby, K. E. et al. Autoimmune and chronic inflammatory disorders and risk of non-Hodgkin lymphoma by subtype. J. Natl Cancer Inst. 98, 51–60 (2006).
Weng, M. Y., Huang, Y. T., Liu, M. F. & Lu, T. H. Incidence of cancer in a nationwide population cohort of 7,852 patients with primary Sjögren's syndrome in Taiwan. Ann. Rheum. Dis. 71, 524–527 (2012).
Johnsen, S. J. et al. Risk of non-hodgkin's lymphoma in primary Sjögren's syndrome: a population-based study. Arthritis Care Res. (Hoboken) 65, 816–821 (2013).
Royer, B. et al. Lymphomas in patients with Sjögren's syndrome are marginal zone B-cell neoplasms, arise in diverse extranodal and nodal sites, and are not associated with viruses. Blood 90, 766–775 (1997).
Voulgarelis, M. et al. Prognosis and outcome of non-Hodgkin lymphoma in primary Sjögren syndrome. Medicine (Baltimore) 91, 1–9 (2012).
Anaya, J. M., McGuff, H. S., Banks, P. M. & Talal, N. Clinicopathological factors relating malignant lymphoma with Sjögren's syndrome. Semin. Arthritis Rheum. 25, 337–346 (1996).
Solans-Laque, R. et al. Risk, predictors, and clinical characteristics of lymphoma development in primary Sjögren's syndrome. Semin. Arthritis Rheum. 41, 415–423 (2011).
Tzioufas, A. G., Boumba, D. S., Skopouli, F. N. & Moutsopoulos, H. M. Mixed monoclonal cryoglobulinemia and monoclonal rheumatoid factor cross-reactive idiotypes as predictive factors for the development of lymphoma in primary Sjögren's syndrome. Arthritis Rheum. 39, 767–772 (1996).
Voulgarelis, M., Dafni, U. G., Isenberg, D. A. & Moutsopoulos, H. M. Malignant lymphoma in primary Sjogren's syndrome: a multicenter, retrospective, clinical study by the European Concerted Action on Sjögren's Syndrome. Arthritis Rheum. 42, 1765–1772 (1999).
Martin, T. et al. Salivary gland lymphomas in patients with Sjögren's syndrome may frequently develop from rheumatoid factor B cells. Arthritis Rheum. 43, 908–916 (2000).
Bende, R. J. et al. Among B cell non-Hodgkin's lymphomas, MALT lymphomas express a unique antibody repertoire with frequent rheumatoid factor reactivity. J. Exp. Med. 201, 1229–1241 (2005).
Theander, E. et al. Lymphoid organisation in labial salivary gland biopsies is a possible predictor for the development of malignant lymphoma in primary Sjögren's syndrome. Ann. Rheum. Dis. 70, 1363–1368 (2011).
Song, H., Tong, D., Cha, Z. & Bai, J. C-X-C chemokine receptor type 5 gene polymorphisms are associated with non-Hodgkin lymphoma. Mol. Biol. Rep. 39, 8629–8635 (2012).
Gottenberg, J. E. et al. Serum levels of beta2-microglobulin and free light chains of immunoglobulins are associated with systemic disease activity in primary Sjögren's syndrome. Data at enrollment in the prospective ASSESS cohort. PLoS ONE 8, e59868 (2013).
Quartuccio, L. et al. BLyS upregulation in Sjögren's syndrome associated with lymphoproliferative disorders, higher ESSDAI score and B-cell clonal expansion in the salivary glands. Rheumatology (Oxford) 52, 276–281 (2013).
Mariette, X. Lymphomas complicating Sjögren's syndrome and hepatitis C virus infection may share a common pathogenesis: chronic stimulation of rheumatoid factor B cells. Ann. Rheum. Dis. 60, 1007–1010 (2001).
Mariette, X. et al. Germinal and somatic abnormalities of the TNFAIP3 gene support a two-hit hypothesis of lymphomagenesis in autoimmune disease [abstract]. Arthritis Rheum. 63 (Suppl. 10), 161 (2011).
Musone, S. L. et al. Sequencing of TNFAIP3 and association of variants with multiple autoimmune diseases. Genes Immun. 12, 176–182 (2011).
Honma, K. et al. TNFAIP3/A20 functions as a novel tumor suppressor gene in several subtypes of non-Hodgkin lymphomas. Blood 114, 2467–2475 (2009).
Novak, U. et al. The NF-κB negative regulator TNFAIP3 (A20) is inactivated by somatic mutations and genomic deletions in marginal zone lymphomas. Blood 113, 4918–4921 (2009).
Nocturne, G. et al. Germinal and somatic genetic variants of TNFAIP3 promote lymphomagenesis process complicating primary Sjögren's syndrome [abstract OP0023]. Ann. Rheum. Dis. 72 (Suppl. 3), 55 (2013).
Cruz-Tapias, P., Rojas-Villarraga, A., Maier-Moore, S. & Anaya, J. M. HLA and Sjögren's syndrome susceptibility. A meta-analysis of worldwide studies. Autoimmun. Rev. 11, 281–287 (2012).
Hagiwara, E., Pando, J., Ishigatsubo, Y. & Klinman, D. M. Altered frequency of type 1 cytokine secreting cells in the peripheral blood of patients with primary Sjögren's syndrome. J. Rheumatol. 25, 89–93 (1998).
Cha, S. et al. A dual role for interferon-γ in the pathogenesis of Sjögren's syndrome-like autoimmune exocrinopathy in the nonobese diabetic mouse. Scand. J. Immunol. 60, 552–565 (2004).
Yin, H. et al. Location of immunization and interferon-γ are central to induction of salivary gland dysfunction in Ro60 peptide immunized model of Sjögren's syndrome. PLoS ONE 6, e18003 (2011).
McGrath-Morrow, S. et al. IL-12 overexpression in mice as a model for Sjögren lung disease. Am. J. Physiol. Lung Cell. Mol. Physiol. 291, L837–L846 (2006).
Vosters, J. L. et al. Interleukin-12 induces salivary gland dysfunction in transgenic mice, providing a new model of Sjögren's syndrome. Arthritis Rheum. 60, 3633–3641 (2009).
Hall, J. C. et al. Precise probes of type II interferon activity define the origin of interferon signatures in target tissues in rheumatic diseases. Proc. Natl Acad. Sci. USA 109, 17609–17614 (2012).
Kariuki, S. N. et al. Cutting edge: autoimmune disease risk variant of STAT4 confers increased sensitivity to IFN-α in lupus patients in vivo. J. Immunol. 182, 34–38 (2009).
Miceli-Richard, C. et al. Interleukin 12 is involved in an interferon type I signature through crosstalk of CD4+ T cells and plasmacytoid dendritic cells [abstract 2321]. Arthritis Rheum. 64 (Suppl. 10), S980 (2012).
Geginat, J., Sallusto, F. & Lanzavecchia, A. Cytokine-driven proliferation and differentiation of human naive, central memory, and effector memory CD4+ T cells. J. Exp. Med. 194, 1711–1719 (2001).
Bikker, A. et al. Increased expression of interleukin-7 in labial salivary glands of patients with primary Sjögren's syndrome correlates with increased inflammation. Arthritis Rheum. 62, 969–977 (2010).
Bikker, A. et al. Increased interleukin (IL)-7Rα expression in salivary glands of patients with primary Sjögren's syndrome is restricted to T cells and correlates with IL-7 expression, lymphocyte numbers and activity. Ann. Rheum. Dis. 71, 1027–1033 (2012).
Bikker, A. et al. Clinical efficacy of leflunomide in primary Sjögren's syndrome is associated with regulation of T-cell activity and upregulation of IL-7 receptor alpha expression. Ann. Rheum. Dis. 71, 1934–1941 (2012).
Katsifis, G. E., Rekka, S., Moutsopoulos, N. M., Pillemer, S. & Wahl, S. M. Systemic and local interleukin-17 and linked cytokines associated with Sjögren's syndrome immunopathogenesis. Am. J. Pathol. 175, 1167–1177 (2009).
Sakai, A., Sugawara, Y., Kuroishi, T., Sasano, T. & Sugawara, S. Identification of IL-18 and TH17 cells in salivary glands of patients with Sjögren's syndrome, and amplification of IL-17-mediated secretion of inflammatory cytokines from salivary gland cells by IL-18. J. Immunol. 181, 2898–2906 (2008).
Christodoulou, M. I., Kapsogeorgou, E. K., Moutsopoulos, N. M. & Moutsopoulos, H. M. Foxp3+ T-regulatory cells in Sjögren's syndrome: correlation with the grade of the autoimmune lesion and certain adverse prognostic factors. Am. J. Pathol. 173, 1389–1396 (2008).
Sarigul, M. et al. The numbers of Foxp3+ TREG cells are positively correlated with higher grade of infiltration at the salivary glands in primary Sjögren's syndrome. Lupus 19, 138–145 (2010).
Gottenberg, J. E. et al. CD4 CD25high regulatory T cells are not impaired in patients with primary Sjögren's syndrome. J. Autoimmun. 24, 235–242 (2005).
Ciccia, F. et al. Potential involvement of IL-22 and IL-22-producing cells in the inflamed salivary glands of patients with Sjögren's syndrome. Ann. Rheum. Dis. 71, 295–301 (2012).
Cella, M., Otero, K. & Colonna, M. Expansion of human NK-22 cells with IL-7, IL-2, and IL-1β reveals intrinsic functional plasticity. Proc. Natl Acad. Sci. USA 107, 10961–10966 (2010).
Miceli-Richard, C. et al. Genetic variation at the NCR3 locus is associated with risk of primary Sjögren's syndrome and implicates a role for NK cells in this autoimmune disease [abstract]. Ann. Rheum. Dis. 70 (Suppl. 3), 212 (2011).
Nocturne, G. et al. Genetic and functional analyses implicate NCR3/NKp30 in the pathogenesis of primary Sjögren's syndrome. Sci. Transl. Med. (in press).
Nordmark, G. et al. Genetic variation in the NCR3 locus is associated with anti-SSA/SSB positive primary Sjögren's syndrome in Scandinavian samples [abstract 522]. Arthritis Rheum. 64 (Suppl. 10), S228 (2012).
Johnson, E. O., Kostandi, M. & Moutsopoulos, H. M. Hypothalamic-pituitary-adrenal axis function in Sjögren's syndrome: mechanisms of neuroendocrine and immune system homeostasis. Ann. NY Acad. Sci. 1088, 41–51 (2006).
Johnson, E. O., Vlachoyiannopoulos, P. G., Skopouli, F. N., Tzioufas, A. G. & Moutsopoulos, H. M. Hypofunction of the stress axis in Sjögren's syndrome. J. Rheumatol. 25, 1508–1514 (1998).
Tzioufas, A. G., Tsonis, J. & Moutsopoulos, H. M. Neuroendocrine dysfunction in Sjögren's syndrome. Neuroimmunomodulation 15, 37–45 (2008).
Ishimaru, N. et al. Development of autoimmune exocrinopathy resembling Sjögren's syndrome in estrogen-deficient mice of healthy background. Am. J. Pathol. 163, 1481–1490 (2003).
Ishimaru, N. et al. Expression of the retinoblastoma protein RbAp48 in exocrine glands leads to Sjögren's syndrome-like autoimmune exocrinopathy. J. Exp. Med. 205, 2915–2927 (2008).
Tsinti, M. et al. Functional estrogen receptors alpha and beta are expressed in normal human salivary gland epithelium and apparently mediate immunomodulatory effects. Eur. J. Oral Sci. 117, 498–505 (2009).
Moutsopoulos, H. M. Sjögren's syndrome: autoimmune epithelitis. Clin. Immunol. Immunopathol. 72, 162–165 (1994).
Robinson, C. P., Yamamoto, H., Peck, A. B. & Humphreys-Beher, M. G. Genetically programmed development of salivary gland abnormalities in the NOD (nonobese diabetic)–SCID mouse in the absence of detectable lymphocytic infiltration: a potential trigger for sialoadenitis of NOD mice. Clin. Immunol. Immunopathol. 79, 50–59 (1996).
Kapsogeorgou, E. K., Moutsopoulos, H. M. & Manoussakis, M. N. Functional expression of a costimulatory B7.2 (CD86) protein on human salivary gland epithelial cells that interacts with the CD28 receptor, but has reduced binding to CTLA4. J. Immunol. 166, 3107–3113 (2001).
Manoussakis, M. N. et al. Expression of B7 costimulatory molecules by salivary gland epithelial cells in patients with Sjögren's syndrome. Arthritis Rheum. 42, 229–239 (1999).
Ittah, M. et al. B cell-activating factor of the tumor necrosis factor family (BAFF) is expressed under stimulation by interferon in salivary gland epithelial cells in primary Sjögren's syndrome. Arthritis Res. Ther. 8, R51 (2006).
van Venrooij, W. J. & Pruijn, G. J. Ribonucleoprotein complexes as autoantigens. Curr. Opin. Immunol. 7, 819–824 (1995).
Kapsogeorgou, E. K., Abu-Helu, R. F., Moutsopoulos, H. M. & Manoussakis, M. N. Salivary gland epithelial cell exosomes: A source of autoantigenic ribonucleoproteins. Arthritis Rheum. 52, 1517–1521 (2005).
Dass, S. et al. Reduction of fatigue in Sjögren syndrome with rituximab: results of a randomised, double-blind, placebo-controlled pilot study. Ann. Rheum. Dis. 67, 1541–1544 (2008).
Meijer, J. M. et al. Effectiveness of rituximab treatment in primary Sjögren's syndrome: a randomized, double-blind, placebo-controlled trial. Arthritis Rheum. 62, 960–968 (2010).
Seror, R. et al. Tolerance and efficacy of rituximab and changes in serum B cell biomarkers in patients with systemic complications of primary Sjögren's syndrome. Ann. Rheum. Dis. 66, 351–357 (2007).
De Vita, S. et al. Efficacy of belimumab on non-malignant parotid swelling and systemic manifestations of Sjögren's syndrome: results of the Beliss study [abstract 2189]. Arthritis Rheum. 64 (Suppl. 10), S926 (2012).
Fernandez, N. C. et al. Dendritic cells directly trigger NK cell functions: cross-talk relevant in innate anti-tumor immune responses in vivo. Nat. Med. 5, 405–411 (1999).
Gerosa, F. et al. Reciprocal activating interaction between natural killer cells and dendritic cells. J. Exp. Med. 195, 327–333 (2002).
Walzer, T., Dalod, M., Robbins, S. H., Zitvogel, L. & Vivier, E. Natural-killer cells and dendritic cells: “l'union fait la force”. Blood 106, 2252–2258 (2005).
Nossent, J. C., Rischmueller, M. & Lester, S. Low copy number of the Fc-gamma receptor 3B gene FCGR3B is a risk factor for primary Sjögren's syndrome. J. Rheumatol. 39, 2142–2147 (2012).
Bolstad, A. I. et al. Association between genetic variants in the tumour necrosis factor/lymphotoxin alpha/lymphotoxin beta locus and primary Sjögren's syndrome in Scandinavian samples. Ann. Rheum. Dis. 71, 981–988 (2012).
Wang, Z. Y., Morinobu, A., Kanagawa, S. & Kumagai, S. Polymorphisms of the mannose binding lectin gene in patients with Sjögren's syndrome. Ann. Rheum. Dis. 60, 483–486 (2001).
Ou, T. T. et al. IκBα promoter polymorphisms in patients with primary Sjögren's syndrome. J. Clin. Immunol. 28, 440–444 (2008).
Anaya, J. M., Correa, P. A., Mantilla, R. D. & Arcos-Burgos, M. TAP, HLA-DQB1, and HLA-DRB1 polymorphism in Colombian patients with primary Sjögren's syndrome. Semin. Arthritis Rheum. 31, 396–405 (2002).
Nordmark, G. et al. Association of EBF1, FAM167A(C8orf13)-BLK and TNFSF4 gene variants with primary Sjögren's syndrome. Genes Immun. 12, 100–109 (2011).
Gomez, L. M. et al. PTPN22 C1858T polymorphism in Colombian patients with autoimmune diseases. Genes Immun. 6, 628–631 (2005).
Petrek, M. et al. CC chemokine receptor 5 and interleukin-1 receptor antagonist gene polymorphisms in patients with primary Sjögren's syndrome. Clin. Exp. Rheumatol. 20, 701–703 (2002).
Hulkkonen, J. et al. Genetic association between interleukin-10 promoter region polymorphisms and primary Sjögren's syndrome. Arthritis Rheum. 44, 176–179 (2001).
Kassan, S. S. et al. Increased risk of lymphoma in sicca syndrome. Ann. Intern. Med. 89, 888–892 (1978).
Valesini, G. et al. Differential risk of non-Hodgkin's lymphoma in Italian patients with primary Sjögren's syndrome. J. Rheumatol. 24, 2376–2380 (1997).
Kauppi, M., Pukkala, E. & Isomaki, H. Elevated incidence of hematologic malignancies in patients with Sjögren's syndrome compared with patients with rheumatoid arthritis (Finland). Cancer Causes Control 8, 201–204 (1997).