Chang, M. H. & Nigrovic, P. A. Antibody-dependent and -independent mechanisms of inflammatory arthritis. JCI Insight 4, https://doi.org/10.1172/jci.insight.125278 (2019).
Gravallese, E. M. & Firestein, G. S. Rheumatoid arthritis — common origins, divergent mechanisms. N. Engl. J. Med. 388, 529–542 (2023).
Google ScholarÂ
Roberts, W. N., Daltroy, L. H. & Anderson, R. J. Stability of normal joint findings in persistent classic rheumatoid arthritis. Arthritis Rheum. 31, 267–271 (1988).
Google ScholarÂ
Chang, M. H. et al. Joint-specific memory and sustained risk for new joint accumulation in autoimmune arthritis. Arthritis Rheumatol. 74, 1851–1858 (2022).
Google ScholarÂ
Chang, M. H. et al. Arthritis flares mediated by tissue-resident memory T cells in the joint. Cell Rep. 37, 109902 (2021).
Google ScholarÂ
Heckert, S. L. et al. Joint inflammation tends to recur in the same joints during the rheumatoid arthritis disease course. Ann. Rheum. Dis. 81, 169–174 (2022).
Google ScholarÂ
Heckert, S. L. et al. Patterns of clinical joint inflammation in juvenile idiopathic arthritis. RMD Open 9, e002941 (2023).
Google ScholarÂ
Gebhardt, T., Palendira, U., Tscharke, D. C. & Bedoui, S. Tissue-resident memory T cells in tissue homeostasis, persistent infection, and cancer surveillance. Immunol. Rev. 283, 54–76 (2018).
Google ScholarÂ
Szabo, P. A., Miron, M. & Farber, D. L. Location, location, location: tissue resident memory T cells in mice and humans. Sci. Immunol. 4, eaas9673 (2019).
Google ScholarÂ
Boniface, K. et al. Vitiligo skin is imprinted with resident memory CD8 T cells expressing CXCR3. J. Invest. Dermatol. 138, 355–364 (2018).
Google ScholarÂ
Richmond, J. M. et al. Resident memory and recirculating memory T cells cooperate to maintain disease in a mouse model of vitiligo. J. Invest. Dermatol. 139, 769–778 (2019).
Google ScholarÂ
Boyman, O. et al. Spontaneous development of psoriasis in a new animal model shows an essential role for resident T cells and tumor necrosis factor-α. J. Exp. Med. 199, 731–736 (2004).
Google ScholarÂ
Samat, A. A. K., van der Geest, J., Vastert, S. J., van Loosdregt, J. & van Wijk, F. Tissue-resident memory T cells in chronic inflammation-local cells with systemic effects? Cells 10, 409 (2021).
Google ScholarÂ
Fonseca, R. et al. Developmental plasticity allows outside-in immune responses by resident memory T cells. Nat. Immunol. 21, 412–421 (2020).
Google ScholarÂ
Wijeyesinghe, S. et al. Expansible residence decentralizes immune homeostasis. Nature 592, 457–462 (2021).
Google ScholarÂ
Mueller, S. N. & Mackay, L. K. Tissue-resident memory T cells: local specialists in immune defence. Nat. Rev. Immunol. 16, 79–89 (2016).
Google ScholarÂ
Heeg, M. & Goldrath, A. W. Insights into phenotypic and functional CD8+ TRM heterogeneity. Immunol. Rev. 316, 8–22 (2023).
Google ScholarÂ
Kumar, B. V. et al. Human tissue-resident memory T cells are defined by core transcriptional and functional signatures in lymphoid and mucosal sites. Cell Rep. 20, 2921–2934 (2017).
Google ScholarÂ
Crowl, J. T. et al. Tissue-resident memory CD8+ T cells possess unique transcriptional, epigenetic and functional adaptations to different tissue environments. Nat. Immunol. 23, 1121–1131 (2022).
Google ScholarÂ
Mackay, L. K. et al. Hobit and Blimp1 instruct a universal transcriptional program of tissue residency in lymphocytes. Science 352, 459–463 (2016).
Google ScholarÂ
Poon, M. M. L. et al. Tissue adaptation and clonal segregation of human memory T cells in barrier sites. Nat. Immunol. 24, 309–319 (2023).
Google ScholarÂ
Christo, S. N. et al. Discrete tissue microenvironments instruct diversity in resident memory T cell function and plasticity. Nat. Immunol. 22, 1140–1151 (2021).
Google ScholarÂ
Lin, Y. H. et al. Small intestine and colon tissue-resident memory CD8+ T cells exhibit molecular heterogeneity and differential dependence on Eomes. Immunity 56, 207–223.e8 (2023).
Google ScholarÂ
Schenkel, J. M. et al. IL-15-independent maintenance of tissue-resident and boosted effector memory CD8 T cells. J. Immunol. 196, 3920–3926 (2016).
Google ScholarÂ
FitzPatrick, M. E. B. et al. Human intestinal tissue-resident memory T cells comprise transcriptionally and functionally distinct subsets. Cell Rep. 34, 108661 (2021).
Google ScholarÂ
Milner, J. J. et al. Heterogenous populations of tissue-resident CD8+ T cells are generated in response to infection and malignancy. Immunity 52, 808–824.e7 (2020).
Google ScholarÂ
Frizzell, H. et al. Organ-specific isoform selection of fatty acid-binding proteins in tissue-resident lymphocytes. Sci. Immunol. 5, https://doi.org/10.1126/sciimmunol.aay9283 (2020).
Pan, Y. et al. Survival of tissue-resident memory T cells requires exogenous lipid uptake and metabolism. Nature 543, 252–256 (2017).
Google ScholarÂ
Howie, D., Ten Bokum, A., Necula, A. S., Cobbold, S. P. & Waldmann, H. The role of lipid metabolism in T lymphocyte differentiation and survival. Front. Immunol. 8, 1949 (2017).
Google ScholarÂ
Jin, R. et al. Role of FABP5 in T cell lipid metabolism and function in the tumor microenvironment. Cancers 15, https://doi.org/10.3390/cancers15030657 (2023).
Steinert, E. M. et al. Quantifying memory CD8 T cells reveals regionalization of immunosurveillance. Cell 161, 737–749 (2015).
Google ScholarÂ
Jung, J. et al. Synovial fluid CD69+CD8+ T cells with tissue-resident phenotype mediate perforin-dependent citrullination in rheumatoid arthritis. Clin. Transl. Immunol. 9, e1140 (2020).
Google ScholarÂ
Guggino, G., Rizzo, A., Mauro, D., Macaluso, F. & Ciccia, F. Gut-derived CD8+ tissue-resident memory T cells are expanded in the peripheral blood and synovia of SpA patients. Ann. Rheum. Dis. 80, e174 (2021).
Google ScholarÂ
Horai, R. et al. Development of chronic inflammatory arthropathy resembling rheumatoid arthritis in interleukin 1 receptor antagonist-deficient mice. J. Exp. Med. 191, 313–320 (2000).
Google ScholarÂ
Zhang, F. et al. Defining inflammatory cell states in rheumatoid arthritis joint synovial tissues by integrating single-cell transcriptomics and mass cytometry. Nat. Immunol. 20, 928–942 (2019).
Google ScholarÂ
Jonsson, A. H. et al. Granzyme K+ CD8 T cells form a core population in inflamed human tissue. Sci. Transl. Med. 14, eabo0686 (2022).
Google ScholarÂ
Petrelli, A. et al. PD-1+CD8+ T cells are clonally expanding effectors in human chronic inflammation. J. Clin. Invest. 128, 4669–4681 (2018).
Google ScholarÂ
Vanni, A. et al. Clonally expanded PD-1-expressing T cells are enriched in synovial fluid of juvenile idiopathic arthritis patients. Eur. J. Immunol. 53, e2250162 (2023).
Google ScholarÂ
Maschmeyer, P. et al. Antigen-driven PD-1+ TOX+ BHLHE40+ and PD-1+ TOX+ EOMES+ T lymphocytes regulate juvenile idiopathic arthritis in situ. Eur. J. Immunol. 51, 915–929 (2021).
Google ScholarÂ
Steel, K. J. A. et al. Polyfunctional, proinflammatory, tissue-resident memory phenotype and function of synovial interleukin-17A+CD8+ T cells in psoriatic arthritis. Arthritis Rheumatol. 72, 435–447 (2020).
Google ScholarÂ
Povoleri, G. A. M. et al. Psoriatic and rheumatoid arthritis joints differ in the composition of CD8+ tissue-resident memory T cell subsets. Cell Rep. 42, 112514 (2023).
Google ScholarÂ
Penkava, F. et al. Single-cell sequencing reveals clonal expansions of pro-inflammatory synovial CD8 T cells expressing tissue-homing receptors in psoriatic arthritis. Nat. Commun. 11, 4767 (2020).
Google ScholarÂ
Qaiyum, Z., Gracey, E., Yao, Y. & Inman, R. D. Integrin and transcriptomic profiles identify a distinctive synovial CD8+ T cell subpopulation in spondyloarthritis. Ann. Rheum. Dis. 78, 1566–1575 (2019).
Google ScholarÂ
Sasson, S. C., Gordon, C. L., Christo, S. N., Klenerman, P. & Mackay, L. K. Local heroes or villains: tissue-resident memory T cells in human health and disease. Cell Mol. Immunol. 17, 113–122 (2020).
Google ScholarÂ
Arazi, A. et al. The immune cell landscape in kidneys of patients with lupus nephritis. Nat. Immunol. 20, 902–914 (2019).
Google ScholarÂ
Zhou, M. et al. JAK/STAT signaling controls the fate of CD8+CD103+ tissue-resident memory T cell in lupus nephritis. J. Autoimmun. 109, 102424 (2020).
Google ScholarÂ
Boothby, I. C. et al. Early-life inflammation primes a T helper 2 cell-fibroblast niche in skin. Nature 599, 667–672 (2021).
Google ScholarÂ
Nygaard, G. & Firestein, G. S. Restoring synovial homeostasis in rheumatoid arthritis by targeting fibroblast-like synoviocytes. Nat. Rev. Rheumatol. 16, 316–333 (2020).
Google ScholarÂ
Bottini, N. & Firestein, G. S. Duality of fibroblast-like synoviocytes in RA: passive responders and imprinted aggressors. Nat. Rev. Rheumatol. 9, 24–33 (2013).
Google ScholarÂ
Nakano, K., Whitaker, J. W., Boyle, D. L., Wang, W. & Firestein, G. S. DNA methylome signature in rheumatoid arthritis. Ann. Rheum. Dis. 72, 110–117 (2013).
Google ScholarÂ
Whitaker, J. W. et al. An imprinted rheumatoid arthritis methylome signature reflects pathogenic phenotype. Genome Med. 5, 40 (2013).
Google ScholarÂ
Ai, R. et al. DNA methylome signature in synoviocytes from patients with early rheumatoid arthritis compared to synoviocytes from patients with longstanding rheumatoid arthritis. Arthritis Rheumatol. 67, 1978–1980 (2015).
Google ScholarÂ
Crowley, T. et al. Priming in response to pro-inflammatory cytokines is a feature of adult synovial but not dermal fibroblasts. Arthritis Res. Ther. 19, 35 (2017).
Google ScholarÂ
Friscic, J. et al. The complement system drives local inflammatory tissue priming by metabolic reprogramming of synovial fibroblasts. Immunity 54, 1002–1021.e10 (2021).
Google ScholarÂ
Friscic, J. et al. Reset of inflammatory priming of joint tissue and reduction of the severity of arthritis flares by bromodomain inhibition. Arthritis Rheumatol. 75, 517–532 (2023).
Google ScholarÂ
Lefevre, S. et al. Synovial fibroblasts spread rheumatoid arthritis to unaffected joints. Nat. Med. 15, 1414–1420 (2009).
Google ScholarÂ
Orange, D. E. et al. RNA identification of PRIME cells predicting rheumatoid arthritis flares. N. Engl. J. Med. 383, 218–228 (2020).
Google ScholarÂ
Frank-Bertoncelj, M. et al. Epigenetically-driven anatomical diversity of synovial fibroblasts guides joint-specific fibroblast functions. Nat. Commun. 8, 14852 (2017).
Google ScholarÂ
Ciurea, A. et al. Joint-level responses to tofacitinib and methotrexate: a post hoc analysis of data from ORAL Start. Arthritis Res. Ther. 25, 185 (2023).
Google ScholarÂ
Kurowska-Stolarska, M. & Alivernini, S. Synovial tissue macrophages in joint homeostasis, rheumatoid arthritis and disease remission. Nat. Rev. Rheumatol. 18, 384–397 (2022).
Google ScholarÂ
Alivernini, S. et al. Distinct synovial tissue macrophage subsets regulate inflammation and remission in rheumatoid arthritis. Nat. Med. 26, 1295–1306 (2020).
Google ScholarÂ
Misharin, A. V. et al. Nonclassical Ly6C− monocytes drive the development of inflammatory arthritis in mice. Cell Rep. 9, 591–604 (2014).
Google ScholarÂ
Culemann, S. et al. Locally renewing resident synovial macrophages provide a protective barrier for the joint. Nature 572, 670–675 (2019).
Google ScholarÂ
Montgomery, A. B. et al. Tissue-resident, extravascular Ly6c− monocytes are critical for inflammation in the synovium. Cell Rep. 42, 112513 (2023).
Google ScholarÂ
Alivernini, S. et al. Synovial features of patients with rheumatoid arthritis and psoriatic arthritis in clinical and ultrasound remission differ under anti-TNF therapy: a clue to interpret different chances of relapse after clinical remission? Ann. Rheum. Dis. 76, 1228–1236 (2017).
Google ScholarÂ
Aegerter, H. et al. Influenza-induced monocyte-derived alveolar macrophages confer prolonged antibacterial protection. Nat. Immunol. 21, 145–157 (2020).
Google ScholarÂ
Guilliams, M. & Svedberg, F. R. Does tissue imprinting restrict macrophage plasticity? Nat. Immunol. 22, 118–127 (2021).
Google ScholarÂ
Hanlon, M. M. et al. Rheumatoid arthritis macrophages are primed for inflammation and display bioenergetic and functional alterations. Rheumatology 62, 2611–2620 (2023).
Google ScholarÂ
Vickovic, S. et al. Three-dimensional spatial transcriptomics uncovers cell type localizations in the human rheumatoid arthritis synovium. Commun. Biol. 5, 129 (2022).
Google ScholarÂ
Iijima, N. & Iwasaki, A. T cell memory. A local macrophage chemokine network sustains protective tissue-resident memory CD4 T cells. Science 346, 93–98 (2014).
Google ScholarÂ
Vu, T. T., Koguchi-Yoshioka, H. & Watanabe, R. Skin-resident memory T cells: pathogenesis and implication for the treatment of psoriasis. J. Clin. Med. 10, https://doi.org/10.3390/jcm10173822 (2021).
Puig, L. et al. The biological basis of disease recurrence in psoriasis: a historical perspective and current models. Br. J. Dermatol. 186, 773–781 (2022).
Google ScholarÂ
Matos, T. R. et al. Clinically resolved psoriatic lesions contain psoriasis-specific IL-17-producing ɑβ T cell clones. J. Clin. Invest. 127, 4031–4041 (2017).
Google ScholarÂ
Li, X., Jiang, M., Chen, X. & Sun, W. Etanercept alleviates psoriasis by reducing the Th17/Treg ratio and promoting M2 polarization of macrophages. Immun. Inflamm. Dis. 10, e734 (2022).
Google ScholarÂ
Mehta, H. et al. Differential changes in inflammatory mononuclear phagocyte and T-cell profiles within psoriatic skin during treatment with guselkumab vs. secukinumab. J. Invest. Dermatol. 141, 1707–1718.e9 (2021).
Google ScholarÂ
Whitley, S. K. et al. Local IL-23 is required for proliferation and retention of skin-resident memory TH17 cells. Sci. Immunol. 7, eabq3254 (2022).
Google ScholarÂ
Dong, C., Lin, L. & Du, J. Characteristics and sources of tissue-resident memory T cells in psoriasis relapse. Curr. Res. Immunol. 4, 100067 (2023).
Google ScholarÂ
Monti, S., Montecucco, C., Bugatti, S. & Caporali, R. Rheumatoid arthritis treatment: the earlier the better to prevent joint damage. RMD Open 1, e000057 (2015).
Google ScholarÂ
Fraenkel, L. et al. 2021 American College of Rheumatology guideline for the treatment of rheumatoid arthritis. Arthritis Care Res. 73, 924–939 (2021).
Boers, M. Understanding the window of opportunity concept in early rheumatoid arthritis. Arthritis Rheum. 48, 1771–1774 (2003).
Google ScholarÂ
van Nies, J. A. et al. What is the evidence for the presence of a therapeutic window of opportunity in rheumatoid arthritis? A systematic literature review. Ann. Rheum. Dis. 73, 861–870 (2014).
Google ScholarÂ
Burgers, L. E., Raza, K. & van der Helm-van Mil, A. H. Window of opportunity in rheumatoid arthritis — definitions and supporting evidence: from old to new perspectives. RMD Open 5, e000870 (2019).
Google ScholarÂ
Nigrovic, P. A. Review: Is there a window of opportunity for treatment of systemic juvenile idiopathic arthritis? Arthritis Rheumatol. 66, 1405–1413 (2014).
Google ScholarÂ
Nigrovic, P. A. et al. Biological classification of childhood arthritis: roadmap to a molecular nomenclature. Nat. Rev. Rheumatol. 17, 257–269 (2021).
Google ScholarÂ
Nigrovic, P. A. et al. Anakinra as first-line disease-modifying therapy in systemic juvenile idiopathic arthritis: report of forty-six patients from an international multicenter series. Arthritis Rheum. 63, 545–555 (2011).
Google ScholarÂ
Ter Haar, N. M. et al. Treatment to target using recombinant interleukin-1 receptor antagonist as first-line monotherapy in new-onset systemic juvenile idiopathic arthritis: results from a five-year follow-up study. Arthritis Rheumatol. 71, 1163–1173 (2019).
Google ScholarÂ
Pardeo, M. et al. Early treatment and IL1RN single-nucleotide polymorphisms affect response to anakinra in systemic juvenile idiopathic arthritis. Arthritis Rheumatol. 73, 1053–1061 (2021).
Google ScholarÂ
Henderson, L. A. et al. Th17 reprogramming of T cells in systemic juvenile idiopathic arthritis. JCI Insight 5, https://doi.org/10.1172/jci.insight.132508 (2020).
Levescot, A. et al. IL-1β-driven osteoclastogenic Tregs accelerate bone erosion in arthritis. J. Clin. Invest. 131, https://doi.org/10.1172/JCI141008 (2021).
Alivernini, S. et al. Inclusion of synovial tissue-derived characteristics in a nomogram for the prediction of treatment response in treatment-naive rheumatoid arthritis patients. Arthritis Rheumatol. 73, 1601–1613 (2021).
Google ScholarÂ
Bergstra, S. A. et al. Earlier is better when treating rheumatoid arthritis: but can we detect a window of opportunity? RMD Open 6, https://doi.org/10.1136/rmdopen-2020-001242 (2020).
Goekoop-Ruiterman, Y. P. et al. Clinical and radiographic outcomes of four different treatment strategies in patients with early rheumatoid arthritis (the BeSt study): a randomized, controlled trial. Arthritis Rheum. 52, 3381–3390 (2005).
Google ScholarÂ
Wevers-de Boer, K. et al. Remission induction therapy with methotrexate and prednisone in patients with early rheumatoid and undifferentiated arthritis (the IMPROVED study). Ann. Rheum. Dis. 71, 1472–1477 (2012).
Google ScholarÂ
Ebrahimian, S. et al. Can treating rheumatoid arthritis with disease-modifying anti-rheumatic drugs at the window of opportunity with tight control strategy lead to long-term remission and medications free remission in real-world clinical practice? A cohort study. Clin. Rheumatol. 40, 4485–4491 (2021).
Google ScholarÂ
Krijbolder, D. I. et al. Intervention with methotrexate in patients with arthralgia at risk of rheumatoid arthritis to reduce the development of persistent arthritis and its disease burden (TREAT EARLIER): a randomised, double-blind, placebo-controlled, proof-of-concept trial. Lancet 400, 283–294 (2022).
Google ScholarÂ
Cope, A. P. et al. Abatacept in individuals at high risk of rheumatoid arthritis (APIPPRA): a randomised, double-blind, multicentre, parallel, placebo-controlled, phase 2b clinical trial. Lancet 403, 838–849 (2024).
Google ScholarÂ
Sugiyama, D. et al. Impact of smoking as a risk factor for developing rheumatoid arthritis: a meta-analysis of observational studies. Ann. Rheum. Dis. 69, 70–81 (2010).
Google ScholarÂ
Anderson, J. J., Wells, G., Verhoeven, A. C. & Felson, D. T. Factors predicting response to treatment in rheumatoid arthritis: the importance of disease duration. Arthritis Rheum. 43, 22–29 (2000).
Google ScholarÂ
Aletaha, D. et al. Effect of disease duration and prior disease-modifying antirheumatic drug use on treatment outcomes in patients with rheumatoid arthritis. Ann. Rheum. Dis. 78, 1609–1615 (2019).
Google ScholarÂ
Kerschbaumer, A. et al. Efficacy of synthetic and biological DMARDs: a systematic literature review informing the 2022 update of the EULAR recommendations for the management of rheumatoid arthritis. Ann. Rheum. Dis. 82, 95–106 (2023).
Google ScholarÂ
Chang, C. Y., Meyer, R. M. & Reiff, A. O. Impact of medication withdrawal method on flare-free survival in patients with juvenile idiopathic arthritis on combination therapy. Arthritis Care Res. 67, 658–666 (2015).
Google ScholarÂ
Guzman, J. et al. The risk and nature of flares in juvenile idiopathic arthritis: results from the ReACCh-Out cohort. Ann. Rheum. Dis. 75, 1092–1098 (2016).
Google ScholarÂ
Simonini, G. et al. Flares after withdrawal of biologic therapies in juvenile idiopathic arthritis: clinical and laboratory correlates of remission duration. Arthritis Care Res. 70, 1046–1051 (2018).
Curtis, J. R. et al. Etanercept or methotrexate withdrawal in rheumatoid arthritis patients in sustained remission. Arthritis Rheumatol. 73, 759–768 (2021).
Google ScholarÂ
Emery, P. et al. Adalimumab dose tapering in patients with rheumatoid arthritis who are in long-standing clinical remission: results of the phase IV PREDICTRA study. Ann. Rheum. Dis. 79, 1023–1030 (2020).
Google ScholarÂ
Ringold, S. et al. Disease recapture rates after medication discontinuation and flare in juvenile idiopathic arthritis: an observational study within the childhood arthritis and rheumatology research alliance registry. Arthritis Care Res. 75, 715–723 (2023).
Richmond, J. M. et al. Antibody blockade of IL-15 signaling has the potential to durably reverse vitiligo. Sci. Transl. Med. 10, https://doi.org/10.1126/scitranslmed.aam7710 (2018).
Hassert, M. et al. Regenerating murine CD8+ lung tissue resident memory T cells after targeted radiation exposure. J. Exp. Med. 221, https://doi.org/10.1084/jem.20231144 (2024).
Schenkel, J. M., Fraser, K. A. & Masopust, D. Cutting edge: resident memory CD8 T cells occupy frontline niches in secondary lymphoid organs. J. Immunol. 192, 2961–2964 (2014).
Google ScholarÂ
Beura, L. K. et al. T cells in nonlymphoid tissues give rise to lymph-node-resident memory T cells. Immunity 48, 327–338.e5 (2018).
Google ScholarÂ
Stolley, J. M. et al. Retrograde migration supplies resident memory T cells to lung-draining LN after influenza infection. J. Exp. Med. 217, https://doi.org/10.1084/jem.20192197 (2020).
Klicznik, M. M. et al. Human CD4+CD103+ cutaneous resident memory T cells are found in the circulation of healthy individuals. Sci. Immunol. 4, https://doi.org/10.1126/sciimmunol.aav8995 (2019).
Mijnheer, G. et al. Compartmentalization and persistence of dominant (regulatory) T cell clones indicates antigen skewing in juvenile idiopathic arthritis. Elife 12, https://doi.org/10.7554/eLife.79016 (2023).
Spreafico, R. et al. A circulating reservoir of pathogenic-like CD4+ T cells shares a genetic and phenotypic signature with the inflamed synovial micro-environment. Ann. Rheum. Dis. 75, 459–465 (2016).
Google ScholarÂ
Leijten, E. F. et al. Tissue-resident memory CD8+ T cells from skin differentiate psoriatic arthritis from psoriasis. Arthritis Rheumatol. 73, 1220–1232 (2021).
Google ScholarÂ
Kunnamo, I., Kallio, P., Pelkonen, P. & Viander, M. Serum-sickness-like disease is a common cause of acute arthritis in children. Acta Paediatr. Scand. 75, 964–969 (1986).
Google ScholarÂ
Lawley, T. J. et al. A prospective clinical and immunologic analysis of patients with serum sickness. N. Engl. J. Med. 311, 1407–1413 (1984).
Google ScholarÂ
Steere, A. C. et al. Treatment of Lyme arthritis. Arthritis Rheum. 37, 878–888 (1994).
Google ScholarÂ
Oen, K. et al. Early predictors of longterm outcome in patients with juvenile rheumatoid arthritis: subset-specific correlations. J. Rheumatol. 30, 585–593 (2003).
Google ScholarÂ
Selvaag, A. M., Aulie, H. A., Lilleby, V. & Flato, B. Disease progression into adulthood and predictors of long-term active disease in juvenile idiopathic arthritis. Ann. Rheum. Dis. 75, 190–195 (2016).
Google ScholarÂ
Lengl-Janssen, B., Strauss, A. F., Steere, A. C. & Kamradt, T. The T helper cell response in Lyme arthritis: differential recognition of Borrelia burgdorferi outer surface protein A in patients with treatment-resistant or treatment-responsive Lyme arthritis. J. Exp. Med. 180, 2069–2078 (1994).
Google ScholarÂ
Steere, A. C. et al. Antibiotic-refractory Lyme arthritis is associated with HLA−DR molecules that bind a Borrelia burgdorferi peptide. J. Exp. Med. 203, 961–971 (2006).
Google ScholarÂ
James, E. A. et al. Citrulline-specific Th1 cells are increased in rheumatoid arthritis and their frequency is influenced by disease duration and therapy. Arthritis Rheumatol. 66, 1712–1722 (2014).
Google ScholarÂ
Nigrovic, P. A. & White, P. H. Care of the adult with juvenile rheumatoid arthritis. Arthritis Rheum. 55, 208–216 (2006).
Google ScholarÂ