Potential infectious agents in the induction of arthritides

Current Opinion in Rheumatology

Volumn 8, Issue 3, 1996, Pages 203-209

  Krause, Andreas ^a   Kamradt, Thomas ^a   Burmester, Gerd R ^a  

^a CHARITÉ UNIVERSITÄTSMEDIZIN BERLIN   (Germany)

Author keywords

[No Author keywords available]

Indexed keywords

ARTHRITIS; ENVIRONMENTAL FACTOR; HEREDITY; HUMAN; IMMUNOPATHOLOGY; PATHOGENESIS; PRIORITY JOURNAL; REVIEW; RHEUMATIC DISEASE; RHEUMATOID ARTHRITIS;

EID: 0029900167     PISSN: 10408711     EISSN: None     Source Type: Journal    
DOI: 10.1097/00002281-199605000-00007     Document Type: Review

References (71)

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11. Naides SJ: Viral arthritis including HIV. Curr Opin Rheumatol 1995, 7:337-342. A good review highlighting current data supporting the role of viral infections in triggering rheumatic diseases.
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19. Perry LL, Wilkerson MJ, Hullinger GA, Cheevers WP: Depressed CD4+ T lymphocyte proliferate response and enhanced antibody response to viral antigen in chronic lentivirus-induced arthritis. J Infect Dis 1995, 171:328-334.
20. Wilkerson MJ, Davis WC, Baszler TV, Cheevers WP: Immunopathology of chronic lentivirus-induced arthritis. Am J Pathol 1995, 146:1433-1443.
21. Ornstein MH, Kerr LD, Spiera H: A reexamination of the relationship between active rheumatoid arthritis and the acquired immunodeficiency syndrome. Arthritis Rheum 1995, 38:1701-1706. An interesting case report on a patient with both active rheumatoid arthritis and AIDS and a review of the literature concerning the coexistence of these two diseases.
22. Bailer RT, Lazo A, Harisdangkul V, Ehrlich GD, Gray LS, Whisler RL, Blakeslee JR: Lack of evidence for human T cell lymphotrophic virus type I or II infection in patients with systemic lupus erythematosus or rheumatoid arthritis. J Rheumatol 1994, 21:2217-2224. Serum antibodies against HTLV-I and II and HIV, reverse transcriptase activity, and HTLV-I and -II gag antigen in PBMC culture supernatants and HTLV-I and -II pro viral sequences in PBMCs were determined in 115 patients with various rheumatic or connective tissue autoimmune diseases. The results did not provide any evidence for an association between HIV or HTLV-I or -II infections and the rheumatic diseases investigated.
23. Nelson PN, Lever AM, Bruckner FE, Isenberg DA, Kessaris N, Hay FC: Polymerase chain reaction fails to incriminate exogenous retroviruses HTLV-I and HIV-I In rheumatological diseases although a minority of sera cross react with retroviral antigens. Ann Rheum Dis 1994, 53:749-754. Although some patients with rheumatoid arthritis, systemic lupus erythematosus, or polymyositis were HTLV-I seropositive, no retroviral sequences could be detected in peripheral blood, synovial tissue, or muscle biopsies by PCR analysis using consensus primers for HTLV-I and HIV-1.
24. Nelson PN, Bowman SJ, Hay FC, Lanchbury JS, Panayi GS, Lever AM: Absence of exogenous retroviruses in Felty's syndrome [letter]. Br J Rheumatol 1995, 34:185-187.
25. Perl A, Colombo E, Dai H, Agarwal R, Mark KA, Banki K, Poiesz BJ, Phillips PE, Hoch SO, Reveille JD, Arnett FC: Antibody reactivity to the HRES-1 endogenous retroviral element identifies a subset of patients with systemic lupus erythematosus and overlap syndromes. Arthritis Rheum 1995, 38:1660-1671. A subset of patients with systemic lupus erythematosus and other autoimmune rheumatic diseases have antibodies against an endogenous retroviral element-encoded nuclear protein autoantigen (HRES-1/p28) that are negatively associated with anti-Ro/La and positively correlated with antiribonucleoprotein autoantibodies. A cross-reactive epitope of HRES-1/p28 and ribonucleoproteins is described. Certain HLA-DQB1 alleles appear to influence the generation of these autoantibodies. This study provides further evidence that antigens encoded by endogenous retroviruses may induce autoimmunity.
26. Cassinotti P, Bas S, Siegl G, Vischer TL: Association between human parvovirus B19 infection and arthritis. Ann Rheum Dis 1995, 54:498-500.
27. Gran JT, Johnsen V, Myklebust G, Nordbo SA: The variable clinical picture of arthritis induced by human parvovirus B19: report of seven adult cases and review of the literature. Scand J Rheumatol 1995, 24:174-179.
28. Kerr JR, Cartron JP, Curran MD, Moore JE, Elliott JRM, Mollan RAB: A study of the role of parvovirus B19 in rheumatoid arthritis. Br J Rheumatol 1995, 34:809-813. Parvovirus B19 DNA was detected at the same frequency in the synovial membrane of patients with rheumatoid arthritis and patients with osteoarthritis. Thus, the results do not support the involvement of parvovirus B19 in the etiopathogenesis of rheumatoid arthritis.
29. Tsai YT, Chiang BL, Kao YF, Hsieh KH: Detection of Epstein-Barr virus and cytomegalovirus genome in white blood cells from patients with juvenile rheumatoid arthritis and childhood systemic lupus erythematosus. Int Arch Allergy Immunol 1995, 106:235-240.
30. Newkirk MM, Watanabe Duffy KN, Leclerc J, Lambert N, Shiroky JB: Detection of cytomegalovirus, Epstein-Barr virus and herpes virus-6 in patients with rheumatoid arthritis with or without Sjögren's syndrome. Br J Rheumatol 1994, 33:317-322.
31. Nikkari S, Luukkainen R, Nikkari L, Skurnik M, Toivanen P: No evidence of adenoviral hexon regions in rheumatoid synovial cells and tissue. J Rheumatol 1994, 21:2179-2183.
32. Berthelot JM, Besse B, Billaudel S, Delecrin J, Letenneur J, Youinou P, Maugars Y, Prost A: Search of papillomavirus genome in synovial membranes and rheumatoid nodules [in French]. Rev Rhum Ed Fr 1994, 61:491-496.
33. Kloppenburg M, Breedveld FC, Terwiel JP, Mallee C, Dijkmans BA: Minocycline in active rheumatoid arthritis: a double-blind, placebo-controlled trial. Arthritis Rheum 1994, 37:629-636. This study shows small but interesting beneficial effects of minocycline in patients with rheumatoid arthritis. An important finding was marked decreases in laboratory parameters such as inflammation and rheumatoid factor.
34. Kloppenburg M, Mattie H, Douwes N, Dijkmans BA, Breedveld FC: Minocycline in the treatment of rheumatoid arthritis: relationship of serum concentrations to efficacy. J Rheumatol 1995, 22:611-616.
35. Tilley BC, Alarcón GS, Heyse SP, Trentham DE, Neuner R, Kaplan DA, Clegg DO, Leisen JC, Buckley L, Cooper SM, et al.: Minocycline in rheumatoid arthritis: a 48-week, double-blind, placebo-controlled trial. Ann Intern Med 1995, 122:81-89. This larger study corroborates the results reported by Kloppenburg et al. (Arthritis Rheum 1994, 37:629-636).
36. Tilley BC, Alarcón GS, Heyse SP, Trentham DE, Neuner R, Kaplan DA, Clegg DO, Leisen JC, Buckley L, Cooper SM, et al.: Minocycline in rheumatoid arthritis: a 48-week, double-blind, placebo-controlled trial. Ann Intern Med 1995, 122:81-89. This larger study corroborates the results reported by Kloppenburg et al. (Arthritis Rheum 1994, 37:629-636).
37. Kjeldsen Kragh J, Rashid T, Dybwad A, Sioud M, Haugen M, Forre O, Ebringer A: Decrease in anti-Proteus mirabilis but not anti-Escherichia coli antibody levels in rheumatoid arthritis patients treated with fasting and a one year vegetarian diet. Ann Rheum Dis 1995, 54:221-224.
38. Kjeldsen Kragh J, Haugen M, Borchgrevink CF, Forre O: Vegetarian diet for patients with rheumatoid arthritis-status: two years after introduction of the diet. Clin Rheumatol 1994, 13:475-482.
39. Eerola E, Mottonen T, Hannonen P, Luukkainen R, Kantola I, Vuori K, Tuominen J, Toivanen P: Intestinal flora in early rheumatoid arthritis. Br J Rheumatol 1994, 33:1030-1038.
40. Senior BW, McBride PD, Morley KD, Kerr MA: The detection of raised levels of IgM to Proteus mirabilis in sera from patients with rheumatoid arthritis. J Med Microbiol 1995, 43:176-184.
41. Wilson C, Ebringer A, Ahmadi K, Wrigglesworth J, Tiwana H, Fielder M, Binder A, Ettelaie C, Cunningham P, Joannou C, Bansal S: Shared amino acid sequences between major histocompatibility complex class II glycoproteins, type XI collagen and Proteus mirabilis in rheumatoid arthritis. Ann Rheum Dis 1995, 54:216-220.
42. Ford DK, Schulzer M: Synovial lymphocytes indicate "bacterial" agents may cause some cases of rheumatoid arthritis. J Rheumatol 1994, 21:1447-1449.
43. Anderton SM, van der Zee R, Prakken B, Noordzij A, van Eden W: Activation of T cells recognizing self 60-kD heat shock protein can protect against experimental arthritis. J Exp Med 1995, 181:943-952. Previous work had shown that immunization with mycobacterial hsp protects rats against adjuvant arthritis and other experimentally induced arthritides. The authors' earlier work had identified nine peptide epitopes on mycobacterial hsp65 recognized by rat T cells, only one of which (encompassing amino acids 265 to 270) induced cross-reactive T cells recognizing rat hsp60. This paper reports experiments testing the nine hsp65 peptides for their ability to mediate the protective effect seen with complete mycobacterial hsp65. Only a peptide containing 265 to 270 epitope, inducing self-reactive T cells, mediated protection. This careful analysis shows that the induction of self-reactive T cells does not necessarily imply the induction of autoimmune disease. In contrast, such self-reactive T cells can mediate protection, presumably via immunoregulatory mechanisms.
44. de Graeff Meeder ER, van Eden W, Rijkers GT, Prakken BJ, Kuis W, Voorhorst Ogink MM, van der Zee R, Schuurman HJ, et al.: Juvenile chronic arthritis: T cell reactivity to human HSP60 in patients with a favorable course of arthritis. J Clin Invest 1995, 95:934-940. Building on the findings reported by Anderton et al. (J Exp Med 1995, 181:943-952), the authors analyzed synovial fluid and PBMC proliferation in response to human hsp60 in 23 patients with juvenile arthritis and seven controls. Reactivity to human hsp60 was mostly, but not exclusively, found in patients with a remitting course of the disease, ie, the subgroup of HLA-B27-negative patients with disease of oligoarticular onset. Although epitope mapping was not performed, this work supports the authors' conclusion that self-reactive T cells sometimes mediate protection rather than autoimmune disease.
45. de Graeff Meeder ER, van Eden W, Rijkers GT, Prakken BJ, Kuis W, Voorhorst Ogink MM, van der Zee R, Schuurman HJ, et al.: Juvenile chronic arthritis: T cell reactivity to human HSP60 in patients with a favorable course of arthritis. J Clin Invest 1995, 95:934-940. Building on the findings reported by Anderton et al. (J Exp Med 1995, 181:943-952), the authors analyzed synovial fluid and PBMC proliferation in response to human hsp60 in 23 patients with juvenile arthritis and seven controls. Reactivity to human hsp60 was mostly, but not exclusively, found in patients with a remitting course of the disease, ie, the subgroup of HLA-B27-negative patients with disease of oligoarticular onset. Although epitope mapping was not performed, this work supports the authors' conclusion that self-reactive T cells sometimes mediate protection rather than autoimmune disease.
46. Jalal H, Millar M, Linton C, Dieppe P: Absence of Mycobacterium tuberculosis DNA in synovial fluid from patients with rheumatoid arthritis. Ann Rheum Dis 1994, 53:695-698.
47. Gray J, Marsh PJ, Walker DJ: A search for bacterial DNA in RA synovial fluid using polymer chain reaction. Br J Rheumatol 1994, 33:997-998.
48. Vaughan JH, Valbracht JR, Nguyen MD, Handley HH, Smith RS, Patrick K, Rhodes GH: Epstein-Barr virus-induced autoimmune responses: I. Immunoglobulin M autoantibodies to protein mimicking and not mimicking Epstein-Barr virus nuclear antigen-1. J Clin Invest 1995, 95:1306-1315. First of two studies (see Vaughan et al., J Clin Invest 1995, 95:1316-1327). Excellent study characterizing autoantigens recognized by IgM autoantibodies evolving during Epstein-Barr infections. The authors describe a glycine-rich 28-mer that represents a newly identified, evolutionary conserved autoepitope that is cross-reactive with an Epstein-Barr nuclear antigen-II epitope.
49. Vaughan JH, Valbracht JR, Nguyen MD, Handley HH, Smith RS, Patrick K, Rhodes GH: Epstein-Barr virus-induced autoimmune responses: I. Immunoglobulin M autoantibodies to protein mimicking and not mimicking Epstein-Barr virus nuclear antigen-1. J Clin Invest 1995, 95:1306-1315. First of two studies (see Vaughan et al., J Clin Invest 1995, 95:1316-1327). Excellent study characterizing autoantigens recognized by IgM autoantibodies evolving during Epstein-Barr infections. The authors describe a glycine-rich 28-mer that represents a newly identified, evolutionary conserved autoepitope that is cross-reactive with an Epstein-Barr nuclear antigen-II epitope.
50. Vaughan JH, Nguyen MD, Valbracht JR, Patrick K, Rhodes GH: Epstein-Barr virus-Induced autoimmune responses: II: Immunoglobulin G autoantibodies to mimicking and nonmimicking epitopes: presence in autoimmune disease. J Clin Invest 1995, 95:1316-1327. In the second part of the study (see Vaughan et al., J Clin Invest 1995, 95:1306-1315), the authors describe IgG autoantibodies against the 28-mer autoepitope that were detected only in patients with various autoimmune diseases including rheumatoid arthritis, systemic lupus erythematosus, and chronic inflammatory bowel diseases, but not in patients with infectious mononucleosis. It is concluded that a normally existing inability to generate IgG autoantibodies against this mimicking epitope may be overcome in autoimmune diseases.
51. Vaughan JH, Nguyen MD, Valbracht JR, Patrick K, Rhodes GH: Epstein-Barr virus-Induced autoimmune responses: II: Immunoglobulin G autoantibodies to mimicking and nonmimicking epitopes: presence in autoimmune disease. J Clin Invest 1995, 95:1316-1327. In the second part of the study (see Vaughan et al., J Clin Invest 1995, 95:1306-1315), the authors describe IgG autoantibodies against the 28-mer autoepitope that were detected only in patients with various autoimmune diseases including rheumatoid arthritis, systemic lupus erythematosus, and chronic inflammatory bowel diseases, but not in patients with infectious mononucleosis. It is concluded that a normally existing inability to generate IgG autoantibodies against this mimicking epitope may be overcome in autoimmune diseases.
52. Kamradt T, Krause A, Burmester GR: A role for T-cells in the pathogenesis of treatment-resistant Lyme arthritis? Mol Med 1995, 1:486-490.
53. Bas S, Griffais R, Kvien TK, Glennas A, Melby K, Vischer TL: Amplification of plasmid and chromosome Chlamydia DNA in synovial fluid of patients with reactive arthritis and undifferentiated seronegative oligoarthropathies. Arthritis Rheum 1995, 38:1005-1013.
54. Nanagara R, Li F, Beutler A, Hudson A, Schumacher HR Jr: Alteration of Chlamydia trachomatis biologic behavior in synovial membranes: suppression of surface antigen production in reactive arthritis and Reiter's syndrome. Arthritis Rheum 1995, 38:1410-1417.
55. Viitanen AM, Arstila TP, Lahesmaa R, Granfors K, Skurnik M, Toivanen P: Application of the polymerase chain reaction and immunofluorescence techniques to the detection of bacteria in Yersinia-triggered reactive arthritis [see comments]. Arthritis Rheum 1991, 34:89-96.
56. Nikkari S, Merilahti Palo R, Saario R, Soderstrom KO, Granfors K, Skurnik M, Toivanen P: Versinia-triggered reactive arthritis: use of polymerase chain reaction and immunocytochemical staining in the detection of bacterial components from synovial specimens. Arthritis Rheum 1992, 35:682-687.
57. Nocton JJ, Dressier F, Rutledge BJ, Rys PN, Persing DH, Steere AC: Detection of Borrelia burgdorferi DNA by polymerase chain reaction in synovial fluid from patients with Lyme arthritis. N Engl J Med 1994, 330:229-234.
58. Bradley JF, Johnson RC, Goodman JL: The persistence of spirochetal nucleic acids in active Lyme arthritis [see comments]. Ann Intern Med 1994, 120:487-489.
59. Bloom BJ, Aversa JM, Steere AC: Lack of Borrelia burgdorferi DNA by PCR in synovium after antibiotic treatment in patients with chronic Lyme arthritis arthritis [abstract]. Arthritis Rheum 1995, 38:S345.
60. Matyniak JE, Reiner SL: T helper phenotype and genetic susceptibility in experimental Lyme disease. J Exp Med 1995, 181:1251-1254. This paper describes findings that are very similar to the more extensive data described by Keane-Myers and Nickell (J Immunol 1995, 155:2020-2028).
61. Matyniak JE, Reiner SL: T helper phenotype and genetic susceptibility in experimental Lyme disease. J Exp Med 1995, 181:1251-1254. This paper describes findings that are very similar to the more extensive data described by Keane-Myers and Nickell (J Immunol 1995, 155:2020-2028).
62. Keane-Myers A, Nickell SP: Role of IL-4 and IFN-garnma in modulation of immunity to Borrelia burgdorferi in mice. J Immunol 1995, 155:2020-2028. The authors compared the in vitro cytokine production induced by B. burgdorferi in arthritis-susceptible and arthritis-resistant mice. T cells from susceptible mice produced significantly more interferon gamma and less interleukin-4 than T cells from resistant mice. These results were confirmed in vivo: treatment of either strain with neutralizing antibodies against interleukin-4 led to increased joint swelling and higher spirochete burdens in joints compared with control mice. Treatment with neutralizing antibodies against interferon gamma had the opposite effect.
63. Miller LC, Lynch EA, Isa S, Logan JW, Dinarello CA, Steere AC: Balance of synovial fluid IL-1 beta and IL-1 receptor antagonist and recovery from Lyme arthritis. Lancet 1993, 341:146-148.
64. Chomarat P, Vannier E, Dechanet J, Rissoan MC, Banchereau J, Dinarello CA, Miossec P: Balance of IL-1 receptor antagonist/IL-1 beta In rheumatoid synovium and Its regulation by IL-4 and IL-10. J Immunol 1995, 154:1432-1439.
65. Gahring LC, Weigle WO: The regulatory effects of cytokines on the induction of a peripheral immunologic tolerance in mice. J Immunol 1990, 145:1318-1323.
66. Lengl-Janßen B, Strauss AF, Steere AC, 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 1994, 180:2069-2078. This group examined large numbers of T cell lines from the synovial fluid or blood of patients with treatment-responsive or treatment-resistant Lyme arthritis for the recognition of five different B. burgdorferi proteins. One of these proteins, OspA, was preferentially recognized by T cell lines from patients with treatment-resistant arthritis, but only rarely recognized by T cell lines from patients with treatment-responsive arthritis. The authors conclude that the T cell response against OspA may be involved in the pathogenesis of treatment-resistant Lyme arthritis.
67. Kamradt T, Lengl-Janßen B, Strauss AF, Bansal G, Steere AC: Dominant recognition of a Borrelia burgdoferi outer surface protein A-peptide by T helper cells in patients with treatment-resistant Lyme arthritis. Infect Immun 1996, 64:1284-1289. Building on their earlier work demonstrating differential recognition of OspA (Leng-Janßen et al., J Exp Med 1994, 180:2069-2078), the authors mapped the epitopes of OspA-specific T cell lines and T cell clones from patients with treatment-resistant Lyme arthritis. The region of OspA contained within amino acid residues 84-113 was dominantly recognized. The authors conclude that if the T cell response against OspA is involved in the pathogenesis of treatment-resistant Lyme arthritis, an epitope within OspA residues 84-113 is a potentially arthritogenic epitope.
68. Kamradt T, Lengl-Janßen B, Strauss AF, Bansal G, Steere AC: Dominant recognition of a Borrelia burgdoferi outer surface protein A-peptide by T helper cells in patients with treatment-resistant Lyme arthritis. Infect Immun 1996, 64:1284-1289. Building on their earlier work demonstrating differential recognition of OspA (Leng-Janßen et al., J Exp Med 1994, 180:2069-2078), the authors mapped the epitopes of OspA-specific T cell lines and T cell clones from patients with treatment-resistant Lyme arthritis. The region of OspA contained within amino acid residues 84-113 was dominantly recognized. The authors conclude that if the T cell response against OspA is involved in the pathogenesis of treatment-resistant Lyme arthritis, an epitope within OspA residues 84-113 is a potentially arthritogenic epitope.
69. Hammer J, Gallazzi F, Bono E, Karr RW, Guenot J, Valsasnini P, Nagy ZA, Sinigaglia F: Peptide binding specificity of HLA-DR4 molecules: correlation with rheumatoid arthritis association. J Exp Med 1995, 181:1847-1855. The authors asked whether the "shared epitope" sequence of rheumatoid arthritis-associated HLA-DR β chains imparts a specific pattern of peptide binding. The peptide binding specificities of two rheumatoid arthritis-associated molecules, DRB1*0401 and DRB1*0404, were compared with the closely related but not rheumatoid arthritis-associated DRB1*0402 molecules. The authors found striking differences between the rheumatoid arthritis-associated and nonassociated allotypes. Most differences could be attributed to a single amino acid change at position 71 of the DRβ chain, affecting the charge of residues potentially contacting position 71. The observed patterns allowed the prediction of peptide sequences derived from natural proteins that bind selectively to rheumatoid arthritis-associated DR molecules and not to the unlinked DR molecule. The authors note that this finding should facilitate the identification of antigenic peptides involved in the pathogenesis of rheumatoid arthritis.
70. Fugger L, Rothbard JB, Sønderstrup-McDevitt G: Specificity of a HLA-DRB1*0401 restricted T cell response to type II collagen. Eur J Immunol 1996, 26:928-933. A panel of HLA-DRB 1*0401 restricted murine T cell hybridomas specific for bovine type II collagen were generated from transgenic mice expressing HLA-DRB1*0401 and human CD4. A peptide determinant corresponding to residues 261-273 was immunodominant. This study demonstrates how these transgenic mice can be used to identify a T cell epitope in potential autoantigens.
71. Wucherpfennig KW, Strominger JL: Molecular mimicry in T cell-mediated autoimmunity: viral peptides activate human T cell clones specific for myelin basic protein. Cell 1995, 80:695-705. The authors build on their earlier work in which they determined an immunodominant epitope on myelin basic protein. Subsequently they defined which amino acid residues contained in this epitope were necessary for MHC binding and which were essential for interaction with the T cell receptor. Using this information they did a refined database search and came up with more than 140 potential molecular mimics. Seven of these peptides activated DR2-restricted myelin basic protein-specific human T cell clones, thus opening the possibility of addressing the question of molecular mimicry directly. Interestingly, only one of these potential mimics would have been identified by simple sequence alignment with myelin basic protein.