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(Journal of Leukocyte Biology. 2001;69:331-339.)
© 2001 by Society for Leukocyte Biology

Lymphoid neogenesis: de novo formation of lymphoid tissue in chronic inflammation through expression of homing chemokines

Peter Hjelmström

Department of Medicine, Karolinska Institute, Stockholm, Sweden

Correspondence: Dr. Peter Hjelmström, Karolinska Institutet, Department of Medicine, Rheumatology Unit, Karolinska Hospital CMM L8:04, SE-171 76 Stockholm, Sweden. E-mail: peter.hjelmstrom{at}medks.ki.se


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ABSTRACT
 
Chronic inflammation is a complex pathophysiological process with accumulation of mononuclear cells seen in response to invading pathogens, neoplastic transformation, or autoimmune recognition of self-antigens. The inflammatory process has evolved to facilitate effective elimination of pathogens and tumors and it is normally transient and turned off when the causative stimulus has been eliminated. Occasionally, however, the process is sustained for a long time and can lead to severe tissue damage. This is seen in organ-specific autoimmune diseases such as rheumatoid arthritis, Sjögren’s syndrome, and Hashimoto’s thyroiditis, but also in infectious diseases such as Helicobacter pylori-induced gastritis. Disturbingly, many of these chronic inflammatory diseases are associated with an increased risk for neoplastic transformation and development of lymphomas. This review summarizes experimental evidence suggesting that chronic inflammation involves ectopic de novo formation of organized lymphoid tissue and that this lymphoid neogenesis is regulated by expression of homing chemokines.

Key Words: autoimmune diseases • lymphoma • CXCL13/CXCR5 • CCL21/CCR7 • germinal centers • high endothelial venules


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INTRODUCTION
 
Chronic inflammation is a necessary, albeit often unappreciated, component of host defense that frequently leads to tissue damage. The chronic inflammatory response is heterogeneous and generates different types of cellular infiltrates depending on factors such as antigenic stimulus and affected tissue. Chronic inflammatory infiltrates that morphologically resemble the secondary lymphoid organs lymph nodes (LNs), Peyer’s patches (PPs), and spleen have long been observed and named tertiary lymphoid organs [1 ].


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TUMOR NECROSIS FACTOR (TNF) PROTEINS WERE THE FIRST DISCOVERED MEDIATORS OF LYMPHOID NEOGENESIS
 
The molecular mechanisms behind organization of chronic inflammatory lesions into lymphoid tissue were not studied until Ruddle and colleagues showed that it could be induced by the same signals as those involved in lymphoid organogenesis during development [2 ]. They consequently named the process of de novo formation of organized lymphoid tissue in chronic inflammation lymphoid neogenesis. Lymphotoxin-{alpha} (LT{alpha}; TNF-ß), a member of the TNF family that has been found to be crucial for development of secondary lymphoid organs during ontogeny, ectopically expressed in transgenic mice under the rat insulin promoter (RIP), induced chronic inflammatory infiltrates closely resembling LNs with respect to both cellular composition and organization [2 ]. RIP-LT{alpha} infiltrates were furthermore characterized by presence of activated postcapillary lymphoid blood vessels; high endothelial venules (HEVs), and an increased expression of adhesion molecules mediating homing of naive lymphocytes in secondary lymphoid organs, such as mucosal addressin cell adhesion molecule (MAdCAM) and peripheral LN addressin (PNAd). These morphological characteristics strongly suggest that a de novo formation of lymphoid tissue can be induced by ectopic expression of LT{alpha}, but the infiltrates still needs to be evaluated with regard to functional characteristics such as antigen-presenting capabilities. LT{alpha} and other members of the TNF family contribute both to inflammation and lymphoid organ development through induction of adhesion molecules, chemokines, and other cytokines in complex interactions with the TNFR1 (p55), TNFR2 (p75), and LTß receptors [reviewed in refs. 3 4 ]. The role of the individual members of the TNF family in lymphoid neogenesis is controversial and has been the focus of a recent review [5 ].


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LYMPHOID NEOGENESIS AND TRANSCRIPTION FACTORS
 
TNF proteins are not the only mediators of lymphoid neogenesis and the whole microenvironment of cytokines and chemokines is probably of importance in development and maintenance of lymphoid tissue in chronic inflammation. Important mediators of lymphoid neogenesis acting downstream of TNF proteins are transcription factors, adhesion molecules, and lymphoid tissue homing chemokines. The transcription factor NF-{kappa}B is induced by TNF proteins and during the last year it was shown that alymphoplasia (aly) mice, which exhibit similar developmental defects of lymphoid tissues as LT{alpha} and LTßR deficient mice [6 ], have a point mutation in the NF-{kappa}B-inducing kinase (NIK) [7 ]. Impaired signal transduction downstream of receptors for the homing chemokine CCL21 (formerly called SLC, 6Ckine, TCA-4, or Exodus-2) explains some of the defects in homing of cells to lymphoid tissues in the aly mice [8 ]. CCL21 has been found to stimulate {alpha}4ß7 (LPAM-1) -mediated adhesion to MadCAM-1 on HEVs [9 ], which is interesting because aly mice show a defect in expression of this adhesion molecule in the spleen [10 ]. Splenectomized aly mice, which completely lack secondary lymphoid organs, do not reject vascularized organ transplants, and crossing these mice to RIP-LT{alpha} mice might be a valuable model to study functional capabilities of transgene-induced lymphoid tissue [11 ]. Other mouse strains rendered genetically deficient for NF-{kappa}B subunits with defects in the microarchitecture of secondary lymphoid organs are p52- and Bcl-3-deficient mice and it has been shown that these mice have reduced expression of another homing chemokine, CXCL13 (formerly called BLC or BCA-1) [12 ]. The receptor for CXCL13, CXCR5 (formerly denoted BLR-1), is a target for both NF-{kappa}B and the transcription factors Oct-2 and Bob-1 [13 , 14 ]. The most likely targets for NF-{kappa}B in lymphoid neogenesis are chemokines, adhesion molecules and members of the TNF family themselves, but further experiments with NF-{kappa}B knockout mice or inhibitors of NF-{kappa}B proteins are necessary to identify the precise targets. In addition, there are probably still undiscovered mediators of lymphoid neogenesis both dependent on and independent of TNF signaling. It will be of great interest to identify these specific signals to analyze whether there are several, perhaps redundant, pathways leading to different types of lymphoid neogenesis in different tissues through further experiments with crossed genetically manipulated mice.


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LYMPHOID NEOGENESIS AND HOMING CHEMOKINES
 
In the last year, substantial advances were made in our understanding of how the development and organization of lymphoid follicles depend upon molecular signals from homing chemokines [for recent reviews see refs. 15 16 17 18 19 ]. In particular, the chemokines CXCL13 and CCL21 have been the focus of intense interest. TNF proteins, and in particular the membrane-bound molecule LT{alpha}1ß2, a cytokine that promotes development of follicular dendritic cells (FDCs), are required for normal expression of both CXCL13 and CCL21 [20 ]. Furthermore, gene profiling experiments show that these chemokines are differentially expressed in mice with deficiencies in TNF proteins [21 ]. Expression of CXCL13 and CCL21 is induced in the newly formed lymphoid tissue in the pancreas of RIP-LT{alpha} mice through interaction between the soluble LT{alpha}3 homotrimer and the TNFR1 receptor [22 ]. The most convincing evidence for direct roles of CXCL13 and CCL21 in lymphoid neogenesis in vivo have been shown by studies of transgenic mice expressing these chemokines under the RIP in the pancreas. Ectopic expression of either CXCL13 [23 ] or CCL21 [24 ] triggers lymphoid neogenesis and leads to a de novo formation of organized lymphoid tissue in a similar fashion as seen in RIP-LT{alpha} mice. It is important to note that the infiltrating lymphocytes in RIP-CXCL13 and RIP-CCL21 expressed less activation markers than in RIP-LT{alpha} mice, indicating that lymphocyte activation is not a prerequisite for lymphoid neogenesis.

CXCL13 is constitutively produced by stromal cells in lymphoid tissues and attracts naive B cells and certain activated and memory T cells in vitro [25 26 27 28 ]. The specific receptor for CXCL13, CXCR5, is primarily expressed on mature B lymphocytes and Burkitt’s lymphoma cells [29 30 31 32 33 34 ]. Mice genetically deficient in either CXLC13 or CXCR5 lack most inguinal and peripheral LNs, possess few or abnormal PPs, and have a disorganized spleen [35 , 36 ]. The membrane-bound molecule LT{alpha}1ß2 is required for normal expression of CXCL13 in lymphoid tissues [20 ], and a major recent advance is the finding that CXCL13 induces B cells to up-regulate LT{alpha}1ß2, thereby establishing a positive-feedback loop that is important for follicle development and homeostasis [23 , 35 ]. Cyster and colleagues propose a role for CXCL13 in LN and PP development by recruiting CXCR5+CD3-IL7R+ cells, which have been found to accumulate very early during the development of secondary lymphoid organs [37 38 39 ], and inducing them to express LT{alpha}1ß2 [35 , 40 ]. These cells have been shown to express the transcriptional repressor Id2 and the orphan nuclear hormone receptor ROR{gamma}, and mice lacking these proteins have impaired development of secondary lymphoid organs and lack this cell population [38 , 41 , 42 ]. The presence of CXCR5+CD3-IL7R+ cells, Id2, and ROR{gamma} in lymphoid neogenesis has not been studied so far. The CXCL13-mediated feedback loop appears to be overridden in germinal centers because these develop after immunization with a T cell-dependent antigen both in mice deficient in CXCL13 [35 ] and CXCR5 [43 ]. In germinal centers of CXCL13-deficient mice, B cells expressing LT{alpha}1ß2 are found and this indicates that other signals, which probably are T cell-derived such as CD40-CD40 ligand interaction, drive development and maintenance of FDCs in secondary follicles [35 ]. It is interesting that FDCs do not develop in the lymphoid neogenesis seen in the pancreas of RIP-CXCL13 mice [23 ] and the CXCL13 protein appears, as initially thought, not to be expressed by FDCs [44 ]. Nevertheless, failure to form germinal centers in mice rendered deficient in CD28 signaling and up-regulation of OX40 after immunization have been associated with a lack of CXCR5 on CD4+ T cells [45 ]. The cellular sources of CXCL13 and other mediators of lymphoid neogenesis are still unknown, but likely candidates include B cells [23 ], dendritic cells [46 ], and epithelial mesenchymal cells [47 ]. Further research is needed to identify the mechanisms leading to development of FDCs and secondary follicles.

CCL21 is a unique CC-chemokine containing six cysteines expressed in HEVs and by cells in the T cell zone of lymphoid tissues [48 49 50 51 52 ]. It is primarily a ligand for the CCR7 receptor (previously called EBI1) [53 54 55 56 ], even though it has been reported to bind other chemokine receptors [57 , 58 ]. CCR7 primarily directs the migration of naive T cells and dendritic cells [59 60 61 62 63 64 65 66 67 68 69 70 71 72 73 74 75 76 ], but it is also expressed on a subset of memory T cells that home to LNs upon stimulation [77 , 78 ] and on CD56+CD16- NK cells [79 ]. CCR7 sorts TH1 and TH2 cells in lymphoid tissues [80 ], arrests T cells on HEVs in LNs [81 ] and PPs [82 ], and may dictate the actions of T cells in response to agonist MHC-peptide complexes [83 ]. High expression of CCR7 has been found on adult T cell leukemia (ATL) cells from patients with lymphoid organ involvement of the cancer, indicating that CCL21 might mediate tumor expansion and vascularization [84 ]. This is interesting because inflammation with a follicular pattern and HEVs has been observed in some human cancers, and the presence of CCL21 has not been studied in these diseases [85 ]. In contrast, CCL21 has been found to effectively mediate T cell-dependent antitumor responses in vivo when injected into tumors [86 ] and the mouse C26 colon carcinoma tumor cell line showed reduced tumorigenicity through angiostatic, CD8+ T cell-mediated and NK-mediated tumor resistance mechanisms when transduced with a cDNA encoding CCL21 [87 ]. The bearing of these results for lymphoid neogenesis is not clear and it will be interesting to study the susceptibility of CCL21-deficient mice to neoplastic diseases. In addition, studies of CCR7-deficient mice have shown that the receptor is required for coordination of the primary adaptive immune response and delayed-type hypersensitivity (DTH) reactions by bringing together lymphocytes and dendritic cells to form the characteristic microarchitecture of secondary lymphoid organs [88 ]. Treatment with an anti-CCL21 antibody can inhibit contact-hypersensitivity T cell-dependent DTH reactions induced by hapten sensitization in the skin by interfering with dendritic cell trafficking [89 ]. The mouse strain DDD/1 carries an autosomal recessive mutation designated paucity of lymph node T cells (plt) and have reduced numbers of T cells in the peripheral LN, PP, and spleen [90 ]. Gunn and co-workers showed that plt mice lack expression of CCL21 in lymphoid organs and have defects in both T cell homing and dendritic cell localization [91 ] and the genetic defect in plt mice has indeed been shown to be a deletion of one of two CCL21 genes in the mouse genome [92 ].

Expression of CXCL13 and CCL21 has been found in some human diseases and disease models of chronic inflammation characterized by lymphoid neogenesis. Both CXCL13 and CCL21 are found in the newly formed lymphoid tissue in the pancreas of RIP-LT{alpha} mice and in the insulitis seen in prediabetic non-obese diabetic (NOD) mice [22 ]. CXCL13 are found also in the human diseases Helicobacter pylori-induced chronic gastritis [93 ], Sjögren’s syndrome, and rheumatoid arthritis (Fig. 1 ) [unpublished observations]. The expression of these homing chemokines appears so far to be specific to inflammation characterized by lymphoid neogenesis, and CCL21 expression has for instance not been found in human atherosclerotic plaques [94 ].



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  		Figure 1. The homing chemokine CXCL13 is present in lymphoid follicles of patients with rheumatoid arthritis. (A) Immunohistochemical staining of CXCL13 protein (arrows) using a purified IgG1 monoclonal mouse antibody from R & D Systems, in a follicular lymphocytic cell infiltrate (lc) of a patient with chronic rheumatoid arthritis. (B) Control staining of the same section with an isotype-matched mouse monoclonal antibody (Dako). Original magnification x100 in both panels.


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LYMPHOID NEOGENESIS IN AUTOIMMUNE DISEASES
 
Histopathologists have long observed infiltration of target organs with mononuclear cells and presence of lymphoid follicles in chronic inflammatory autoimmune diseases. Söderström and colleagues found in the beginning of the 1970s that the thyroid gland in patients with Hashimoto’s thyroiditis was organized into a structure that closely resembled a LN, with the presence of germinal centers, large number of plasma cells, and HEVs [95 ], findings subsequently confirmed by other groups [96 , 97 ]. They could also show the presence of ectopic lymphoid follicles with HEVs in the thymus of some patients with the antibody-mediated autoimmune disease myasthenia gravis (MG) [98 ]. It has later been shown that the autoantigen in MG, the nicotinic acetylcholine receptor, is naturally present in the thymus and that germinal centers in the thymus of MG patients contain activated B lymphocytes and plasma cells that produce antibodies against this autoantigen [99 ]. Different mechanism leading to intrathymic development of autoreactive B cell clones in MG have been proposed, including high intrathymic expression of CD23 [100 ] and failure to down-regulate the Bcl-2 protein in the thymic germinal centers [101 ]. Removal of the thymus, thymectomy, is a standard treatment of MG and the clinical signs of muscle weakness ameliorates in many patients after this treatment, indicating a functional role of the ectopic lymphoid tissue in the autoimmune reaction [102 ].

Lymphoid neogenesis is also a characteristic of a number of other human autoimmune diseases (see Table 1 ). In multiple sclerosis, organized lymphoid tissue has been found in the lesions of the central nervous system [103 ]. The rheumatoid disease Sjögren’s syndrome has been shown to be characterized by both morphological and functional features of lymphoid neogenesis, such as presence of HEVs [104 ], dendritic cells and FDCs [105 , 106 ], and antigen-driven clonal proliferation of B cells and lymphoid follicles with clonally expanded lymphocytes [107 108 109 ]. It is interesting that a gene-modified mouse strain deficient in the molecular adaptor Cbl-b spontaneously develops lymphoid structures in primarily the salivary glands and it will be interesting to determine whether this mouse strain has other features of lymphoid neogenesis such as expression of homing chemokines [110 ]. In the salivary gland inflammation of patients with Sjögren’s syndrome expression of both the homing chemokine CXCL13 and its receptor CXCR5 have been observed [unpublished observations]. Rheumatoid arthritis is the human disease where lymphoid neogenesis has been most extensively studied. As early as 1964, Ziff compared the inflamed rheumatic synovial tissue with a LN where primary immunization occurs [111 ], and extensive morphological evidence for lymphoid neogenesis in rheumatoid arthritis has since been accumulated [112 113 114 115 116 117 118 119 120 121 ]. In addition, strong functional evidence suggests that de novo formation of a lymphoid organ occurs in chronic synovial inflammation in rheumatoid arthritis. B cell diversification and somatic hypermutation of antibodies occur in lymphoid follicles in the inflamed joint [118 , 122 ] and Berek and colleagues recently showed that plasma cells develop in synovial germinal centers in rheumatoid arthritis [123 ]. These findings strongly suggest that naive B cells are activated by antigens directly in germinal center reactions in ectopic lymphoid tissue in the synovia. Both CD8+ T cells expressing the CD40 ligand and professional antigen-presenting cells such as dendritic cells appear to play an important role in the formation of these germinal centers in synovitis [119 ]. Preliminary data indicate that the homing chemokine CXCL13 is present in synovial follicles of patients with rheumatoid arthritis (Fig. 1) [unpublished observations]. It is important to note, however, that rheumatoid arthritis, like the other autoimmune diseases, is heterogeneous and that not all patients have morphological evidence of lymphoid neogenesis [124 125 126 ]. Clearly, other mechanisms must lead to sustained arthritis in many patients.


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  		Table 1. Human Chronic Inflammatory Diseases with Lymphoid Neogenesis


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LYMPHOID NEOGENESIS IN INFECTIOUS DISEASES
 
Lymphoid neogenesis has not only been found in autoimmune diseases, but also in some chronic infectious diseases. Intrahepatic lymphoid nodules with functional germinal centers can often be seen in chronic hepatitis C [127 128 129 130 ] and chronic Lyme synovitis has been found to closely resemble LNs with HEVs [131 ]. Gastric infection with Helicobacter pylori induces formation of lymphoid tissue in the gastric mucosa, and this lymphoid neogenesis has also been associated with development of primary gastric mucosa-associated lymphoid tissue (MALT) B cell lymphomas [93 , 132 133 134 135 136 ]. It is interesting that Mazzuccheli and colleagues link lymphoid neogenesis and development of MALT lymphomas in Helicobacter pylori gastritis to expression of CXCL13 [93 ].


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LYMPHOID NEOGENESIS AND DEVELOPMENT OF LYMPHOMAS
 
Chronic inflammation with lymphoid neogenesis seems to be able to induce neoplastic transformation of lymphocytes from ectopic germinal centers leading to, in particular, B cell MALT-lymphomas [137 ]. Autoimmune diseases that have been associated with a highly increased risk for development of lymphomas include for instance Hashimoto’s thyroiditis [138 , 139 ], rheumatoid arthritis [140 ], Sjögren’s syndrome [109 , 141 , 142 ], and celiac disease [143 , 144 ]. Chronic inflammatory infectious diseases are also associated with an increased risk for neoplastic transformation, best exemplified in Helicobacter pylori-induced gastritis as mentioned above. Low-grade B cell MALT-lymphomas developed against a background of chronic inflammation seem to be T cell-dependent because they respond to autologous T cell help [145 ] and express co-stimulatory molecules [146 ]. Continuous antigen stimulation has been shown to be crucial for these lymphomas as they regress in their early stages upon eradication of the antigenic stimulus [147 148 149 150 ]. The hypothesis that MALT lymphomagenesis in its early steps require antigen stimulation is furthermore supported by findings of a restricted immunoglobulin VH gene repertoire and ongoing Ig gene hypermutation in salivary gland MALT lymphomas associated with Sjögren’s syndrome myoepithelial sialadenitis [151 ]. A continuous antigen drive leading to lymphoid neogenesis and formation of lymphoid tissue in a microenvironment where normal regulatory mechanisms probably are absent thus seem to be able to cause both autoimmunity and neoplastic transformation.


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THE PHYSIOLOGICAL AND PATHOLOGICAL ROLE OF LYMPHOID NEOGENESIS
 
A geographical view of immune reactivity, in which an immune response depends upon antigen reaching and being available in secondary lymphoid organs in a dose- and time-dependent manner, was recently proposed by Zinkernagel and co-workers [46 , 152 , 153 ]. In some forms of chronic inflammation, this geographical view is reversed and ectopic lymphoid tissue is formed close to the antigen in the peripheral solid tissue where antigens are available in sufficient concentration and during time enough to promote antigen presentation and immune reactions. Lymphoid neogenesis might provide a focal region where interactions between immune cells, antigen-bearing cells, and pathogens can proceed potentially more efficiently than in normal lymphoid organs. The physiological role for lymphoid neogenesis is, however, so far unknown and as the reaction occurs in a microenvironment where normal mechanisms that should operate to prevent the expansion and maturation of autoreactive T and B cells probably are absent there is a risk for autoimmunity and neoplastic transformation. A local infection or cell-destruction in an adult animal might lead to a burst of previously ignored self-antigens, which directly triggers lymphoid neogenesis and autoimmune reactions in tissues where the self-antigen is continuously expressed. Many autoimmune diseases show a predilection for specific organs and it is possible that autoimmune reactions can be induced and sustained only in tissues where self-antigens are continuously expressed in an appropriate cytokine and chemokine milieu for differentiation of HEVs and initiation of lymphoid neogenesis. Chronic inflammation induced by T cell-mediated cytokine signals in transgenic animals differs in various tissues, and a caveat of the present studies of lymphoid neogenesis is that most experiments have been done of pancreatic inflammation that is characterized by infiltration of mononuclear cells and expression of chemokines specific for Th1 lymphocytes [154 ]. Future experiments with other promoters than the RIP will allow a more precise delineation of tissue and cell-specific factors in lymphoid neogenesis. Another limitation with the present studies using genetically manipulated mice is the lack of experiments using conditionally regulated knockouts and transgenes that would allow kinetic analysis of lymphoid neogenesis in the adult animal. Furthermore, an increasing number of other candidate proteins important for lymphoid organogenesis and differentiation of HEVs during development wait to be studied in vivo in transgenic and knockout models of lymphoid neogenesis and chronic inflammation.


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CONCLUSION
 
Evidence has accumulated that some forms of chronic inflammation can be viewed as a form of lymphoid neogenesis and that TNF proteins and homing chemokines play important roles in this process. Continuous antigen presentation might be the driving force behind lymphoid neogenesis and subsequent development of germinal center-derived lymphomas. From a clinical point of view this emphasizes the need to detect and suppress the antigenic drive aggressively to prevent malignant transformation. Removal of the antigen is already a therapeutic approach in, for instance, celiac disease or Helicobacter pylori-induced gastritis, whereas the therapy for most other diseases with lymphoid neogenesis traditionally is based upon general immunosuppression. In recent years, however, new specific immunomodulatory therapies have been developed targeting in particular the TNF family of proteins, and it is still unknown whether these therapies will inhibit lymphoid neogenesis or development of lymphomas. Our expanding knowledge about homing chemokines and other molecular mediators of lymphoid neogenesis give hope for development of new and more specific therapeutics for chronic inflammatory diseases.


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ACKNOWLEDGEMENTS
 
This study was supported by the Jeansson Foundation, the Swedish Rheumatism Association, the King Gustaf V’s 80-year Foundation and the Karolinska Institute. The author thanks Helena Hildenwall for technical assistance and Nancy H. Ruddle and Åke Lernmark for valuable discussions.

Received August 2, 2000; revised October 21, 2000; accepted October 25, 2000.


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