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Автор: Grafiati
Опубліковано: 10 грудня 2022
Оновлено: 28 січня 2023

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1

Šimelyte, Egle, Marja Rimpiläinen, Leena Lehtonen, Xiang Zhang, and Paavo Toivanen. "Bacterial Cell Wall-Induced Arthritis: Chemical Composition and Tissue Distribution of Four Lactobacillus Strains." Infection and Immunity 68, no. 6 (June 1, 2000): 3535–40. http://dx.doi.org/10.1128/iai.68.6.3535-3540.2000.

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ABSTRACT To study what determines the arthritogenicity of bacterial cell walls, cell wall-induced arthritis in the rat was applied, using four strains of Lactobacillus. Three of the strains used proved to induce chronic arthritis in the rat; all were Lactobacillus casei. The cell wall of Lactobacillus fermentum did not induce chronic arthritis. All arthritogenic bacterial cell walls had the same peptidoglycan structure, whereas that of L. fermentum was different. Likewise, all arthritogenic cell walls were resistant to lysozyme degradation, whereas the L. fermentum cell wall was lysozyme sensitive. Muramic acid was observed in the liver, spleen, and lymph nodes in considerably larger amounts after injection of an arthritogenicL. casei cell wall than following injection of a nonarthritogenic L. fermentum cell wall. The L. casei cell wall also persisted in the tissues longer than theL. fermentum cell wall. The present results, taken together with those published previously, underline the possibility that the chemical structure of peptidoglycan is important in determining the arthritogenicity of the bacterial cell wall.
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2

Mejía, Carla-Ruth, and Rogelio López-Vélez. "Tropical Arthritogenic Alphaviruses." Reumatología Clínica (English Edition) 14, no. 2 (March 2018): 97–105. http://dx.doi.org/10.1016/j.reumae.2017.01.005.

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3

Rao, Shambhavi, and Adam Taylor. "Arthritogenic Alphavirus Capsid Protein." Life 11, no. 3 (March 11, 2021): 230. http://dx.doi.org/10.3390/life11030230.

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Анотація:
In the past two decades Old World and arthritogenic alphavirus have been responsible for epidemics of polyarthritis, causing high morbidity and becoming a major public health concern. The multifunctional arthritogenic alphavirus capsid protein is crucial for viral infection. Capsid protein has roles in genome encapsulation, budding and virion assembly. Its role in multiple infection processes makes capsid protein an attractive target to exploit in combating alphaviral infection. In this review, we summarize the function of arthritogenic alphavirus capsid protein, and describe studies that have used capsid protein to develop novel arthritogenic alphavirus therapeutic and diagnostic strategies.
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4

Archer, J. R., and M. A. Whelan. "HLA-B27 and effector T cells: arthritogenic peptide or arthritogenic antigen?" Lancet 342, no. 8882 (November 1993): 1307. http://dx.doi.org/10.1016/0140-6736(93)92402-f.

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5

Mostafavi, Helen, Eranga Abeyratne, Ali Zaid, and Adam Taylor. "Arthritogenic Alphavirus-Induced Immunopathology and Targeting Host Inflammation as A Therapeutic Strategy for Alphaviral Disease." Viruses 11, no. 3 (March 22, 2019): 290. http://dx.doi.org/10.3390/v11030290.

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Анотація:
Arthritogenic alphaviruses are a group of medically important arboviruses that cause inflammatory musculoskeletal disease in humans with debilitating symptoms, such as arthralgia, arthritis, and myalgia. The arthritogenic, or Old World, alphaviruses are capable of causing explosive outbreaks, with some viruses of major global concern. At present, there are no specific therapeutics or commercially available vaccines available to prevent alphaviral disease. Infected patients are typically treated with analgesics and non-steroidal anti-inflammatory drugs to provide often inadequate symptomatic relief. Studies to determine the mechanisms of arthritogenic alphaviral disease have highlighted the role of the host immune system in disease pathogenesis. This review discusses the current knowledge of the innate immune response to acute alphavirus infection and alphavirus-induced immunopathology. Therapeutic strategies to treat arthritogenic alphavirus disease by targeting the host immune response are also examined.
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6

Suhrbier, Andreas, Marie-Christine Jaffar-Bandjee, and Philippe Gasque. "Arthritogenic alphaviruses—an overview." Nature Reviews Rheumatology 8, no. 7 (May 8, 2012): 420–29. http://dx.doi.org/10.1038/nrrheum.2012.64.

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7

Abdelnabi, Rana, and Leen Delang. "Antiviral Strategies against Arthritogenic Alphaviruses." Microorganisms 8, no. 9 (September 7, 2020): 1365. http://dx.doi.org/10.3390/microorganisms8091365.

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Анотація:
Alphaviruses are members of the Togaviridae family that are mainly transmitted by arthropods such as mosquitoes. In the last decades, several alphaviruses have re-emerged, causing outbreaks worldwide. One example is the re-emergence of chikungunya virus (CHIKV) in 2004, which caused massive epidemics in the Indian Ocean region after which the virus dramatically spread to the Americas in late 2013. Besides CHIKV, other alphaviruses, such as the Ross River virus (RRV), Mayaro virus (MAYV), and Venezuelan equine encephalitis virus (VEEV), have emerged and have become a serious public health concern in recent years. Infections with the Old World alphaviruses (e.g., CHIKV, RRV) are primarily associated with polyarthritis and myalgia that can persist for months to years. On the other hand, New World alphaviruses such as VEEV cause mainly neurological disease. Despite the worldwide (re-)emergence of these viruses, there are no antivirals or vaccines available for the treatment or prevention of infections with alphaviruses. It is therefore of utmost importance to develop antiviral strategies against these viruses. We here provided an overview of the reported antiviral strategies against arthritogenic alphaviruses. In addition, we highlighted the future perspectives for the development and the proper use of such antivirals.
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8

Rodríguez-Morales, Alfonso J., Jorge A. Sánchez-Duque, and Juan-Manuel Anaya. "Response to: Tropical Arthritogenic Alphaviruses." Reumatología Clínica (English Edition) 14, no. 4 (July 2018): 245–46. http://dx.doi.org/10.1016/j.reumae.2017.07.004.

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9

Inglis, TimothyJ. "DIETARY LIPOPOLYSACCHARIDES AS ARTHRITOGENIC ANTIGEN?" Lancet 329, no. 8527 (January 1987): 274. http://dx.doi.org/10.1016/s0140-6736(87)90092-4.

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10

Pettipher, E. R., G. A. Higgs, and B. Henderson. "Arthritogenic activity of interleukin 1." Agents and Actions 19, no. 5-6 (December 1986): 337–38. http://dx.doi.org/10.1007/bf01971244.

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11

Helfgott, S. M., R. Dynesius-Trentham, E. Brahn, and D. E. Trentham. "An arthritogenic lymphokine in the rat." Journal of Experimental Medicine 162, no. 5 (November 1, 1985): 1531–45. http://dx.doi.org/10.1084/jem.162.5.1531.

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Анотація:
A type II collagen-specific arthritogenic lymphokine has been identified in the rat. Arthritogenic factor (AF) is a 65 kD protein generated in vitro by T cells from rats with collagen arthritis, and it induces an erosive, proliferative synovitis when injected into the knee joint of syngeneic naive recipients. Complement does not appear to be required. These data identify a potential T cell-mediated effector mechanism in this model, and suggest that AF may function in other inflammatory synovial diseases.
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12

Levi, Laura I., and Marco Vignuzzi. "Arthritogenic Alphaviruses: A Worldwide Emerging Threat?" Microorganisms 7, no. 5 (May 14, 2019): 133. http://dx.doi.org/10.3390/microorganisms7050133.

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Анотація:
Arthritogenic alphaviruses are responsible for a dengue-like syndrome associated with severe debilitating polyarthralgia that can persist for months or years and impact life quality. Chikungunya virus is the most well-known member of this family since it was responsible for two worldwide epidemics with millions of cases in the last 15 years. However, other arthritogenic alphaviruses that are as of yet restrained to specific territories are the cause of neglected tropical diseases: O’nyong’nyong virus in Sub-Saharan Africa, Mayaro virus in Latin America, and Ross River virus in Australia and the Pacific island countries and territories. This review evaluates their emerging potential in light of the current knowledge for each of them and in comparison to chikungunya virus.
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13

Perper, Stuart J., Beth Browning, Linda C. Burkly, Shawn Weng, Cindy Gao, Keith Giza, Lihe Su, et al. "TWEAK Is a Novel Arthritogenic Mediator." Journal of Immunology 177, no. 4 (August 3, 2006): 2610–20. http://dx.doi.org/10.4049/jimmunol.177.4.2610.

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14

Zabriskie, John B., Suresh Kerwar, and Allan Gibofsky. "THE ARTHRITOGENIC PROPERTIES OF MICROBIAL ANTIGENS." Rheumatic Disease Clinics of North America 24, no. 2 (May 1998): 211–26. http://dx.doi.org/10.1016/s0889-857x(05)70005-3.

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15

Komatsu, Noriko, and Hiroshi Takayanagi. "Arthritogenic T cells in autoimmune arthritis." International Journal of Biochemistry & Cell Biology 58 (January 2015): 92–96. http://dx.doi.org/10.1016/j.biocel.2014.11.008.

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16

Zhang, Xiang, Marja Rimpiläinen, Egle Šimelyte, and Paavo Toivanen. "Enzyme Degradation and Proinflammatory Activity in Arthritogenic and Nonarthritogenic Eubacterium aerofaciens Cell Walls." Infection and Immunity 69, no. 12 (December 1, 2001): 7277–84. http://dx.doi.org/10.1128/iai.69.12.7277-7284.2001.

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ABSTRACT Two almost-identical strains of Eubacterium aerofaciens isolated from the normal human gut flora were used. The cell wall (CW) of one strain with a peptidoglycan (PG) type A4α induces chronic arthritis in the rat after a single intraperitoneal injection, whereas CW of the other with PG type A4β induces only a transient acute arthritis. The CW of the arthritogenic E. aerofaciens was a twofold-more-potent stimulator of the proinflammatory cytokines tumor necrosis factor alpha (TNF-α) and monocyte chemoattractant protein 1 (MCP-1) than the nonarthritogenic CW. After degradation with mutanolysin, the capacity of the arthritogenic PG to stimulate production of TNF-α and MCP-1 was significantly increased, whereas that of the nonarthritogenic PG was significantly decreased. In other words, after enzyme degradation the arthritogenic PG had a four- to fivefold-stronger stimulatory capacity than that of the enzyme-treated nonarthritogenic PG. These findings indicate that the arthritogenicity of CW or a PG is not dependent on the enzyme resistance alone but also on how the PG fragments released by enzyme degradation stimulate the production of proinflammatory cytokines.
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17

de Carvalho Cardoso, Rafaella, Bismarck Rezende, Allan Kardec Nogueira Alencar, Fabrícia Lima Fontes-Dantas, and Guilherme Carneiro Montes. "Role of Arbovirus Infection in Arthritogenic Pain Manifestation—A Systematic Review." Tropical Medicine and Infectious Disease 7, no. 11 (November 21, 2022): 390. http://dx.doi.org/10.3390/tropicalmed7110390.

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The number of publications on the development of arthritic pain after CHIKV infection is increasing; however, there is still a gap in the pathophysiological mechanisms that explain these outcomes. In this review, we conducted a descriptive analysis of the findings of patients to understand their prognosis and to explore therapeutic options. Here, we searched the Cochrane, BVS, PubMed, and Scielo databases using the keywords “arthritis”, “pain”, “arbovirus”, “disease”, “arthritogenic”, and “arthralgia” during the 2000 to 2022 period. Descriptive analyses were conducted to understand the association between CHIKV infection and arthritogenic pain. The present study shows the persistence of acute phase signals for months, making the chronic phase still marked by the presence of arthralgia, often disabling under stimuli, such as temperature variation. CHIKV infection appears to be remarkably similar to rheumatoid arthritis, since both diseases share common symptoms. Once diagnosed, patients are mostly treated with analgesics, nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and disease modifying anti-rheumatic drugs (DMARD). As there are no prophylactic measures or specific treatments for arboviruses, this study gathered information on the development and manifestations of arthritogenic pain.
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18

Zare, Fariba, Maria Bokarewa, Nancy Nenonen, Thomas Bergström, Lena Alexopoulou, Richard A. Flavell, and Andrej Tarkowski. "Arthritogenic Properties of Double-Stranded (Viral) RNA." Journal of Immunology 172, no. 9 (April 20, 2004): 5656–63. http://dx.doi.org/10.4049/jimmunol.172.9.5656.

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19

Maccioni, Mariana, Gabrielle Zeder-Lutz, Haochu Huang, Claudine Ebel, Philippe Gerber, Josiane Hergueux, Patricia Marchal, et al. "Arthritogenic Monoclonal Antibodies from K/BxN Mice." Journal of Experimental Medicine 195, no. 8 (April 15, 2002): 1071–77. http://dx.doi.org/10.1084/jem.20011941.

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Arthritis in the K/BxN mouse model is provoked by pathogenic antibodies (Abs) directed against a ubiquitously expressed protein, glucose-6-phosphate isomerase (GPI). To begin dissecting the repertoire of arthritogenic immunoglobulins (Igs) in the K/BxN model, and to provide a basis for comparison with RA patientswe have generated anti-GPI monoclonal Abs (mAbs) from spontaneously activated B cells in the lymphoid organs of arthritic mice. B cell clones with anti-GPI specificities were present at extraordinarily high frequencies in the spleen, and less frequently in other lymphoid organs and in the synovial fluid. None of the anti-GPI mAbs induced arthritis when injected individually into healthy recipients, but most were effective when combined in pairs or larger pools. Arthritogenic combinations depended on mAbs of the IgG1 isotype, which bound to GPI with Kd in the 10−9 M range, with no indication of cooperative binding between complementing pairs. Pathogenicity was not associated with recognition of a particular epitope, but the ability to form mAb/GPI multimers by simultaneous recognition of different epitopes was clearly required, consistent with the known role of complement and FcRs in this model. Sequence analysis revealed structural similarities amongst the mAbs, indicating that a particular subset of B cells may evade tolerance in K/BxN mice, and that affinity maturation by somatic mutation likely takes place. These results confirm that GPI itself, rather than a cross-reactive molecule, is the target of pathogenic Igs.
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20

Jenkins, Marc K., and Daniel Mueller. "On the trail of arthritogenic T cells." Arthritis & Rheumatism 63, no. 10 (September 27, 2011): 2851–53. http://dx.doi.org/10.1002/art.30440.

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21

Helfgott, S. M., R. I. Kieval, F. C. Breedveld, E. Brahn, C. T. Young, R. Dynesius-Trentham, and D. E. Trentham. "Detection of arthritogenic factor in adjuvant arthritis." Journal of Immunology 140, no. 6 (March 15, 1988): 1838–43. http://dx.doi.org/10.4049/jimmunol.140.6.1838.

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Abstract An evocation of arthritis by an Ag-specific lymphokine has recently been considered with the description of arthritogenic factor (AF) in rats with collagen arthritis. Because rats with CFA-induced arthritis also exhibit T cell reactivity to native type II collagen, T cell lines specific for this protein were established from CFA-injected rats. Supernatant material from these lines contained a type II collagen-binding lymphokine with functional and biochemical attributes identical with those described for AF, i.e., it was a 65-kDa species cross-reacting immunoprotein possessing the ability to incite an erosive, proliferative synovitis when injected into the knee joint of naive recipients. Similarities were also observed with HPLC and on two-dimensional gels. Lymph node cells from rats with arthritis created by injection of the synthetic adjuvant, CP-20,961 failed to produce AF, suggesting that this material is not a ubiquitous concomitant of inflammatory arthritis in the rat. Test injections into sites contiguous with the ear cartilage plate and into fibroblast-lined s.c. pouches suggested that cartilage was a requisite for the induction of inflammation by AF. These data identify a potentially shared effector pathway in the collagen and adjuvant models. The presence of AF in two frequently used models further supports the hypothesis that Ag-specific lymphokines can create autoimmune disease.
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22

Šimelyte, E., P. Isomäki, M. Rimpiläinen, X. Zhang, and P. Toivanen. "Cytokine Production in Arthritis Susceptible and Resistant Rats: A Study with Arthritogenic and Non-arthritogenic Lactobacillus Cell Walls." Scandinavian Journal of Immunology 53, no. 2 (February 2001): 132–38. http://dx.doi.org/10.1046/j.1365-3083.2001.00846.x.

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23

Cremer, M. A., K. Terato, J. M. Seyer, W. C. Watson, G. O. O'Hagan, A. S. Townes, and A. H. Kang. "Immunity to type XI collagen in mice. Evidence that the alpha 3(XI) chain of type XI collagen and the alpha 1(II) chain of type II collagen share arthritogenic determinants and induce arthritis in DBA/1 mice." Journal of Immunology 146, no. 12 (June 15, 1991): 4130–37. http://dx.doi.org/10.4049/jimmunol.146.12.4130.

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Abstract To determine whether native bovine type XI collagen (BXI) is arthritogenic, five strains of inbred mice were immunized with BXI/CFA. Arthritis was not observed in any of these strains, though it was prevalent in DBA/1 and B10.RIII controls immunized with bovine type II collagen (BII). Antisera from BXI-immunized mice reacted with mouse type XI collagen (MsXI), weakly with the alpha-chains of BXI, and minimally with mouse type II collagen (MsII). However, antisera to BII reacted with MsII and MsXI, indicating antibodies to conformation-independent epitopes shared by alpha 1(II) and alpha 3(XI). Mice immunized with BXI containing a small amount of BII developed arthritis much like those immunized with BII; sera from these mice reacted with MsXI and MsII. Delayed-type hypersensitivity responses differed from IgG responses, i.e., BXI elicited responses to alpha 1(XI), alpha 2(XI), alpha 3(XI), and alpha 1(II); BII, to alpha 3(XI) and alpha 1(II) exclusively. To determine whether alpha 1(XI), alpha 2(XI), alpha 3(XI), and alpha 1(II) are arthritogenic, DBA/1J mice were immunized with each alpha-chain. Arthritis was seen in mice injected with alpha 3(XI) or alpha 1(II). Sera to both alpha-chains reacted similarly with MsII and peptide fragment alpha 1(II)-CB11. Epitope mapping using polyclonal and mAb to type II collagen revealed that all polyclonal and 11 of 14 mAb reacted with alpha 3(XI) and alpha 1(II), whereas three mAb reacted only with alpha 1(II). In conclusion, BXI is immunogenic but not arthritogenic in five strains of mice, whereas alpha 3(XI) and alpha 1(II) are arthritogenic and immunogenic in DBA/1 mice and share greater than or equal to 11 epitopes recognized by autoantibody.
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24

Fu, Jiaqi, Song Ling, Ying Liu, Margaret Hannah, Chaim Gilon, and Joseph Holoshitz. "A small shared epitope-mimetic compound potently accelerates osteoclast-mediated bone damage in autoimmune arthritis (P3090)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 43.8. http://dx.doi.org/10.4049/jimmunol.190.supp.43.8.

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Abstract We have recently proposed that the shared epitope (SE) may contribute to rheumatoid arthritis (RA) pathogenesis by acting as a ligand that activates pro-arthritogenic signal transduction events. In order to examine this hypothesis, here we determined the arthritogenic effect of a novel small SE-mimetic compound, c(HS4-4). In this study, we show that c(HS4-4), containing the SE primary sequence motif QKRAA, interacted with the SE receptor calreticulin, potently activated reactive oxygen species (ROS) and nitric oxide (NO) production and markedly facilitated OC differentiation and function in vitro. The pro-osteoclastogenic potency of c(HS4-4) was 100,000 to 1,000,000-fold higher than the potency of a recently described linear SE peptidic ligand. When administered at low-nanogram doses to collagen-induced arthritis (CIA) mice, c(HS4-4) significantly facilitated arthritis onset, increased disease incidence and severity, augmented bone destruction, and increased OC abundance in synovial tissues and osteoclastogenic propensities of bone marrow-derived cells. In conclusion, c(HS4-4), a small SE-mimetic compound with drug-like properties, potently activates OC-mediated bone damage and disease severity in inflammatory arthritis. These findings support the hypothesis that the SE acts as signal transduction ligand that activates an arthritogenic pathway, and attest to the druggability of this pathway.
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25

Glant, Tibor T., Edit I. Buzás, Alison Finnegan, Gabriela Negroiu, Gabriella Cs-Szabó, and Katalin Mikecz. "Critical Roles of Glycosaminoglycan Side Chains of Cartilage Proteoglycan (Aggrecan) in Antigen Recognition and Presentation." Journal of Immunology 160, no. 8 (April 15, 1998): 3812–19. http://dx.doi.org/10.4049/jimmunol.160.8.3812.

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Abstract Systemic immunization of BALB/c mice with proteoglycan (aggrecan) from fetal human cartilage induces progressive polyarthritis, an experimental disease similar to human rheumatoid arthritis. The development of the disease in this genetically susceptible murine strain is based on cross-reactive immune responses between the immunizing fetal human and mouse self-proteoglycans. One of the cross-reactive and arthritogenic T cell epitopes (92GR/QVRVNSA/IY) is localized in the G1 domain of human/murine proteoglycan. Susceptible BALB/c mice, however, develop arthritis only if both the chondroitin sulfate (CS) and keratan sulfate (KS) side chains of the arthritogenic human proteoglycans are removed. The function of these two glycosaminoglycan side chains is opposite. The presence of a KS side chain in adult proteoglycan inhibits the recognition of arthritogenic T cell epitopes, prevents the development of T cell response, and protects animals from autoimmune arthritis. In contrast, the depletion of the CS side chain generates clusters of CS stubs and provokes a strong B cell response. These carbohydrate-specific B cells are the most important proteoglycan APC. Taken together, proteoglycan-induced progressive polyarthritis is dictated by three major components: genetic background of the BALB/c strain, highly specific T cell response to epitope(s) masked by a KS chain in aging tissue, and the presence of proteoglycan (CS stub)-specific B cells required for sufficient Ag presentation.
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26

Zhang, Rong, Arthur S. Kim, Julie M. Fox, Sharmila Nair, Katherine Basore, William B. Klimstra, Rebecca Rimkunas, et al. "Mxra8 is a receptor for multiple arthritogenic alphaviruses." Nature 557, no. 7706 (May 2018): 570–74. http://dx.doi.org/10.1038/s41586-018-0121-3.

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27

Zheng, Timothy, Shawn Weng, Suzanne Szak, and Linda Burkly. "Arthritogenic Simulation of Human Synovial Fibroblasts by TWEAK." Clinical Immunology 123 (2007): S156. http://dx.doi.org/10.1016/j.clim.2007.03.085.

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28

McCulloch, J., Y. W. Zhang, G. A. W. Rook, M. Dawson, G. D. Harkiss, E. Peterhans, H. R. Vogt, and P. M. Lydyard. "Glycosylation of lgG during potentially arthritogenic lentiviral infections." Rheumatology International 14, no. 6 (March 1995): 243–48. http://dx.doi.org/10.1007/bf00262090.

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29

Dobritzsch, Doreen, Ingrid Lindh, Hüseyin Uysal, Kutty S. Nandakumar, Harald Burkhardt, Gunter Schneider, and Rikard Holmdahl. "Crystal structure of an arthritogenic anticollagen immune complex." Arthritis & Rheumatism 63, no. 12 (November 29, 2011): 3740–48. http://dx.doi.org/10.1002/art.30611.

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30

Elango, Jeevithan, Camilo Zamora-Ledezma, Baolin Ge, Chunyu Hou, Zhilin Pan, Bin Bao, Carlos Pérez Albacete Martínez, et al. "Paradoxical Duel Role of Collagen in Rheumatoid Arthritis: Cause of Inflammation and Treatment." Bioengineering 9, no. 7 (July 15, 2022): 321. http://dx.doi.org/10.3390/bioengineering9070321.

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Анотація:
In biology, collagen-biomaterial regulates several signaling mechanisms of bone and immune cells involved in tissue repair and any imbalance in collagen turnover may affect the homeostasis of cells, becoming a major cause of several complications. In this case, the administration of oral collagen may play a potential role in returning cells to their normal function. For several decades, the beneficial effects of collagen have been explored widely, and thus many commercial products are available in cosmetics, food, and biomedical fields. For instance, collagen-based-products have been widely used to treat the complications of cartilage-related-disorders. Many researchers are reporting the anti-arthritogenic properties of collagen-based materials. In contrast, collagen, especially type-II collagen (CII), has been widely used to induce arthritis by immunization in an animal-model with or without adjuvants, and the potentially immunogenic-properties of collagen have been continuously reported for a long time. Additionally, the immune tolerance of collagen is mainly regulated by the T-lymphocytes and B-cells. This controversial hypothesis is getting more and more evidence nowadays from both sides to support its mechanism. Therefore, this review links the gap between the arthritogenic and anti-arthritogenic effects of collagen and explored the actual mechanism to understand the fundamental concept of collagen in arthritis. Accordingly, this review opens-up several unrevealed scientific knots of collagen and arthritis and helps the researchers understand the potential use of collagen in therapeutic applications.
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31

Sandenon Seteyen, Anne-Laure, Emmanuelle Girard-Valenciennes, Axelle Septembre-Malaterre, Philippe Gasque, Pascale Guiraud, and Jimmy Sélambarom. "Anti-Alphaviral Alkaloids: Focus on Some Isoquinolines, Indoles and Quinolizidines." Molecules 27, no. 16 (August 10, 2022): 5080. http://dx.doi.org/10.3390/molecules27165080.

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The discovery and the development of safe and efficient therapeutics against arthritogenic alphaviruses (e.g., chikungunya virus) remain a continuous challenge. Alkaloids are structurally diverse and naturally occurring compounds in plants, with a wide range of biological activities including beneficial effects against prominent pathogenic viruses and inflammation. In this short review, we discuss the effects of some alkaloids of three biologically relevant structural classes (isoquinolines, indoles and quinolizidines). Based on various experimental models (viral infections and chronic diseases), we highlight the immunomodulatory effects of these alkaloids. The data established the capacity of these alkaloids to interfere in host antiviral and inflammatory responses through key components (antiviral interferon response, ROS production, inflammatory signaling pathways and pro- and anti-inflammatory cytokines production) also involved in alphavirus infection and resulting inflammation. Thus, these data may provide a convincing perspective of research for the use of alkaloids as immunomodulators against arthritogenic alphavirus infection and induced inflammation.
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32

Mauri, Claudia, David Gray, Naseem Mushtaq, and Marco Londei. "Prevention of Arthritis by Interleukin 10–producing B Cells." Journal of Experimental Medicine 197, no. 4 (February 10, 2003): 489–501. http://dx.doi.org/10.1084/jem.20021293.

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In this study we have shown that activation of arthritogenic splenocytes with antigen and agonistic anti-CD40 gives raise to a B cell population that produce high levels of interleukin (IL)-10 and low levels of interferon (IFN)-γ. Transfer of these B cells into DBA/1-TcR-β-Tg mice, immunized with bovine collagen (CII) emulsified in complete Freund's adjuvant inhibited T helper type 1 differentiation, prevented arthritis development, and was also effective in ameliorating established disease. IL-10 is essential for the regulatory function of this subset of B cells, as the B cells population isolated from IL-10 knockout mice failed to mediate this protective function. Furthermore, B cells isolated from arthritogenic splenocytes treated in vitro with anti–IL-10/anti–IL-10R were unable to protect recipient mice from developing arthritis. Our results suggest a new role of a subset of B cells in controlling T cell differentiation and autoimmune disorders.
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33

Zhang, Xiang, Jane E. Aubin, Tae-Hwan Kim, Ursula Payne, Basil Chiu, and Robert D. Inman. "Synovial Fibroblasts Infected with Salmonella enterica Serovar Typhimurium Mediate Osteoclast Differentiation and Activation." Infection and Immunity 72, no. 12 (December 2004): 7183–89. http://dx.doi.org/10.1128/iai.72.12.7183-7189.2004.

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ABSTRACT The mechanisms whereby arthritogenic organisms may induce cartilage and bone erosions in infection-triggered arthritis remain unknown. In this study, we asked whether an arthritogenic organism could contribute to osteoclast differentiation and activation through regulation of the receptor activator of NF-κB ligand (RANKL) in synovial fibroblasts. Rat synovial fibroblasts were infected in vitro with Salmonella enterica serovar Typhimurium and monitored over time. The expression of RANKL in resting and infected synovial fibroblasts was quantified by reverse transcription-PCR and Western blotting. Osteoclast progenitors, isolated from femurs of 8-week-old rats and cultured in the presence of macrophage colony-stimulating factor, were cocultured with either infected or noninfected synovial fibroblasts for 2 to 4 days. Differentiation and maturation of osteoclasts were determined by morphology and tartrate-resistant acid phosphatase (TRAP) staining and by a bone resorption bioassay. RANKL expression was undetectable in resting synovial fibroblasts but was dose-dependently upregulated in cells after Salmonella infection. Osteoprotegerin was constitutively expressed by synovial fibroblasts and was not upregulated by infection. Further, we observed the formation of multinucleated TRAP-positive cells and formation of bone resorption pits in cocultures of bone marrow-derived osteoclast precursors with synovial fibroblasts infected with Salmonella but not with heat-killed Salmonella or noninfected cells. Arthritogenic bacteria may alter bone structure via synovial fibroblast intermediaries, since infected synovial fibroblasts (i) upregulate RANKL expression and (ii) enhance osteoclast precursor maturation into multinucleated, TRAP-positive, bone-resorbing, osteoclast-like cells. These data provide a link between infection and osteoclastogenesis. A better understanding of infection-mediated osteoclast differentiation and activation may provide new therapeutic strategies for inflammatory joint disease.
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34

Beasley, David WC, and John G. Aaskov. "Challenges for the utilization of vaccines against arthritogenic alphaviruses." Future Virology 11, no. 4 (April 2016): 235–38. http://dx.doi.org/10.2217/fvl-2016-0019.

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35

INMAN, R. D., and B. CHIU. "Comparative microbicidal activity of synovial fluid on arthritogenic organisms." Clinical and Experimental Immunology 104, no. 1 (April 1996): 80–85. http://dx.doi.org/10.1046/j.1365-2249.1996.d01-650.x.

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36

Lin, Tao, Tingting Geng, Andrew G. Harrison, Duomeng Yang, Anthony T. Vella, Erol Fikrig, and Penghua Wang. "CXCL10 Signaling Contributes to the Pathogenesis of Arthritogenic Alphaviruses." Viruses 12, no. 11 (November 2, 2020): 1252. http://dx.doi.org/10.3390/v12111252.

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Анотація:
Emerging and re-emerging arthritogenic alphaviruses, such as Chikungunya virus (CHIKV) and O’nyong nyong virus, cause acute and chronic crippling arthralgia associated with inflammatory immune responses. Approximately 50% of CHIKV-infected patients suffer from rheumatic manifestations that last 6 months to years. However, the physiological functions of individual immune signaling pathways in the pathogenesis of alphaviral arthritis remain poorly understood. Here, we report that a deficiency in CXCL10, which is a chemoattractant for monocytes/macrophages/T cells, led to the same viremia as wild-type animals, but fewer immune infiltrates and lower viral loads in footpads at the peak of arthritic disease (6–8 days post infection). Macrophages constituted the largest immune cell population in footpads following infection, and were significantly reduced in Cxcl10−/− mice. The viral RNA loads in neutrophils and macrophages were reduced in Cxcl10−/− compared to wild-type mice. In summary, our results demonstrate that CXCL10 signaling promotes the pathogenesis of alphaviral disease and suggest that CXCL10 may be a therapeutic target for mitigating alphaviral arthritis.
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37

La Linn, May, Johannes A. Eble, Christoph Lübken, Robert W. Slade, Jyrki Heino, Janet Davies та Andreas Suhrbier. "An arthritogenic alphavirus uses the α1β1 integrin collagen receptor". Virology 336, № 2 (червень 2005): 229–39. http://dx.doi.org/10.1016/j.virol.2005.03.015.

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38

Chen, Weiqiang, Suan-Sin Foo, Natalie A. Sims, Lara J. Herrero, Nicole C. Walsh, and Suresh Mahalingam. "Arthritogenic alphaviruses: new insights into arthritis and bone pathology." Trends in Microbiology 23, no. 1 (January 2015): 35–43. http://dx.doi.org/10.1016/j.tim.2014.09.005.

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39

de los Toyos, J. R., J. Vázquez, A. Sampedro, and C. Hardisson. "Yersinia enterocolitica serotype O:3 is arthritogenic for mice." Microbial Pathogenesis 8, no. 5 (May 1990): 363–70. http://dx.doi.org/10.1016/0882-4010(90)90095-8.

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40

Trentham, David E. "Collagen Arthritis in Rats, Arthritogenic Lymphokines and Other Aspects." International Reviews of Immunology 4, no. 1 (January 1988): 25–33. http://dx.doi.org/10.3109/08830188809044768.

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41

LORENTZEN. "Identification of Arthritogenic Adjuvants of Self and Foreign Origin." Scandinavian Journal of Immunology 49, no. 1 (January 1999): 45–50. http://dx.doi.org/10.1046/j.1365-3083.1999.00463.x.

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42

SINGH, AMIT KUMAR, AMITA AGGARWAL, SMRITI CHAURASIA, and RAMNATH MISRA. "Identification of Immunogenic HLA-B*27:05 Binding Peptides of Salmonella Outer Membrane Protein in Patients with Reactive Arthritis and Undifferentiated Spondyloarthropathy." Journal of Rheumatology 40, no. 2 (January 15, 2013): 173–85. http://dx.doi.org/10.3899/jrheum.110849.

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Анотація:
Objective.Salmonella outer membrane proteins (OMP) are major immunogenic targets to synovial fluid lymphocytes of patients with reactive arthritis (ReA)/undifferentiated spondyloarthropathy (uSpA). Because these patients have genetic predisposition to HLA-B*27 and its subtype HLA-B*27:05, we sought to identify immunogenic HLA-B*27:05-binding salmonella OMP peptides in patients with ReA/uSpA.Methods.A total of 125 HLA-B*27:05-binding salmonella OMP peptides identified using ProPred-I software were synthesized and grouped in 23 pools. The peptide pools, along with crude enteric bacterial lysates and salmonella OMP, were cultured with synovial fluid (SF) or peripheral blood mononuclear cells (PBMC) from 23 patients with ReA/uSpA, 10 with rheumatoid arthritis (RA), and 10 healthy individuals in 96-well culture plates. Proliferation was measured by tritiated thymidine uptake and interferon-γ (IFN-γ) levels in culture supernatant. Individual peptides from pools having significant responses were retested with cryopreserved cells. Immunogenic peptides thus identified were further tested in 5 additional new patients with ReA/uSpA by flow cytometry. A Basic Local Alignment Search Tool program was used to search for similar peptides from a protein bank of arthritogenic bacteria and human protein.Results.Nineteen of 23 SFMC from ReA/uSpA showed a significant proliferative response to salmonella OMP, with minimal response of PBMC (1/10) from ReA/uSpA, SFMC from RA (1/10), or PBMC from controls (1/10). Nine salmonella OMP peptides, QRAEMLPTL, SRSGLNIAL, LRFLYAKSL, RLEGTWVKL, ARCIAPYAL, KLFLTTAAL, YRNSDFFGL, QRPAVRVKL, and YRVGPGDVL, were identified. Response to QRAEMLPTL was seen in 6/7 HLA-B*27:05-positive patients. All immunogenic peptides had sequence similarity with peptides from arthritogenic bacterial proteins, while 5 had similarity with peptides from human proteins.ConclusionNine novel immunogenic OMP peptides binding to HLA-B*27:05 were identified that showed sequence similarity with other arthritogenic bacteria.
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43

Wildner, Gerhild, and Maria Diedrichs-Moehring. "Multiple Autoantigen Mimotopes of Infectious Agents Induce Autoimmune Arthritis and Uveitis in Lewis Rats." Clinical Diagnostic Laboratory Immunology 12, no. 5 (May 2005): 677–79. http://dx.doi.org/10.1128/cdli.12.5.677-679.2005.

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ABSTRACT We found multimolecular antigenic mimicry of arthritogenic autoantigens and peptides from several other “self” or foreign antigens sharing amino acid sequence homologies. Many of these new mimotopes induced arthritis and/or uveitis upon immunization in Lewis rats, indicating a role for multiple antigens in the initiation of a certain autoimmune disease.
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44

Malonis, Ryan J., James T. Earnest, Arthur S. Kim, Matthew Angeliadis, Frederick W. Holtsberg, M. Javad Aman, Rohit K. Jangra, et al. "Near-germline human monoclonal antibodies neutralize and protect against multiple arthritogenic alphaviruses." Proceedings of the National Academy of Sciences 118, no. 37 (September 10, 2021): e2100104118. http://dx.doi.org/10.1073/pnas.2100104118.

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Arthritogenic alphaviruses are globally distributed, mosquito-transmitted viruses that cause rheumatological disease in humans and include Chikungunya virus (CHIKV), Mayaro virus (MAYV), and others. Although serological evidence suggests that some antibody-mediated heterologous immunity may be afforded by alphavirus infection, the extent to which broadly neutralizing antibodies that protect against multiple arthritogenic alphaviruses are elicited during natural infection remains unknown. Here, we describe the isolation and characterization of MAYV-reactive alphavirus monoclonal antibodies (mAbs) from a CHIKV-convalescent donor. We characterized 33 human mAbs that cross-reacted with CHIKV and MAYV and engaged multiple epitopes on the E1 and E2 glycoproteins. We identified five mAbs that target distinct regions of the B domain of E2 and potently neutralize multiple alphaviruses with differential breadth of inhibition. These broadly neutralizing mAbs (bNAbs) contain few somatic mutations and inferred germline–revertants retained neutralizing capacity. Two bNAbs, DC2.M16 and DC2.M357, protected against both CHIKV- and MAYV-induced musculoskeletal disease in mice. These findings enhance our understanding of the cross-reactive and cross-protective antibody response to human alphavirus infections.
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45

Assunção-Miranda, Iranaia, Christine Cruz-Oliveira, and Andrea T. Da Poian. "Molecular Mechanisms Involved in the Pathogenesis of Alphavirus-Induced Arthritis." BioMed Research International 2013 (2013): 1–11. http://dx.doi.org/10.1155/2013/973516.

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Анотація:
Arthritogenic alphaviruses, including Ross River virus (RRV), Chikungunya virus (CHIKV), Sindbis virus (SINV), Mayaro virus (MAYV), O'nyong-nyong virus (ONNV), and Barmah Forest virus (BFV), cause incapacitating and long lasting articular disease/myalgia. Outbreaks of viral arthritis and the global distribution of these diseases point to the emergence of arthritogenic alphaviruses as an important public health problem. This review discusses the molecular mechanisms involved in alphavirus-induced arthritis, exploring the recent data obtained within vitrosystems andin vivostudies using animal models and samples from patients. The factors associated to the extension and persistence of symptoms are highlighted, focusing on (a) virus replication in target cells, and tissues, including macrophages and muscle cells; (b) the inflammatory and immune responses with recruitment and activation of macrophage, NK cells and T lymphocytes to the lesion focus and the increase of inflammatory mediators levels; and (c) the persistence of virus or viral products in joint and muscle tissues. We also discuss the importance of the establishment of novel animal models to test new molecular targets and to develop more efficient and selective drugs to treat these diseases.
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46

Billingham, M. E., S. Carney, R. Butler, and M. J. Colston. "A mycobacterial 65-kD heat shock protein induces antigen-specific suppression of adjuvant arthritis, but is not itself arthritogenic." Journal of Experimental Medicine 171, no. 1 (January 1, 1990): 339–44. http://dx.doi.org/10.1084/jem.171.1.339.

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A recombinant (r)65-kD protein from Mycobacterium leprae, at levels far in excess of those present in whole mycobacteria, was unable to induce arthritis. Even when combined with a synthetic adjuvant, CP20961, to mimic the peptidoglycan adjuvant component of the mycobacterial cell wall, the r65-kD protein failed to induce arthritis. Pretreatment with as little as 1 microgram r65-kD protein protected rats against arthritis induced by M. tuberculosis, but this r65-kD protein was markedly less able to protect against arthritis induced by the synthetic adjuvant, CP20961, or type II collagen. The r65-kD protein appears, therefore, to produce an antigen-specific protection against arthritis induced by bacterial cell walls containing the 65-kD protein. Such protection can be overcome, however, by arthritogenic T lymphocytes, suggesting that protection occurs by preventing clonal proliferation of autoreactive T lymphocytes that are induced by the adjuvant properties of mycobacterial cell walls. How the r65-kD protein abrogates this particular adjuvant activity, and the nature of the arthritogenic self antigen(s), remain to be elucidated.
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47

Choe, Jung-Yoon, Brian Crain, Sarah R. Wu, and Maripat Corr. "Interleukin 1 Receptor Dependence of Serum Transferred Arthritis Can be Circumvented by Toll-like Receptor 4 Signaling." Journal of Experimental Medicine 197, no. 4 (February 10, 2003): 537–42. http://dx.doi.org/10.1084/jem.20021850.

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Inflammatory arthritis is associated with the release of a network of key cytokines. In T cell receptor transgenic K/BxN mice interleukin (IL)-1 plays a key role in joint swelling and destruction, as suggested by the ability of anti–IL-1receptor (IL-1R) antibody treatment to delay the onset and slow the progression of this disease. This mechanism is dependent on the signaling pathway intermediary myeloid differentiation factor 88 (MyD88), such that neither IL-1R nor MyD88-deficient mice developed visually detectable synovitis after transfer of arthritogenic sera. The Toll-like receptors (TLRs) share the same signaling pathway through MyD88 as the IL-1R. The administration of a TLR-4 ligand, lipopolysaccharide, concomitant with arthritogenic serum in IL-1 receptor–deficient mice resulted in acute paw swelling, but not in MyD88-deficient mice. Also, serum transferred arthritis was not sustained in TLR-4 mutant mice compared with controls. These results suggest that innate immune functions via TLR-4 might perpetuate inflammatory mechanisms and bypass the need for IL-1 in chronic joint inflammation.
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48

Wauben, M. H., C. J. Boog, R. van der Zee, I. Joosten, A. Schlief, and W. van Eden. "Disease inhibition by major histocompatibility complex binding peptide analogues of disease-associated epitopes: more than blocking alone." Journal of Experimental Medicine 176, no. 3 (September 1, 1992): 667–77. http://dx.doi.org/10.1084/jem.176.3.667.

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Peptide analogues of disease-associated epitopes were studied for inhibition of experimental allergic encephalomyelitis (EAE) and adjuvant arthritis (AA) in Lewis rats. EAE- and AA-associated analogues were selected as competitors because of their in vitro inhibitory activity on proliferation of encephalitogenic and arthritogenic T cells. Although the EAE-associated competitor had a superior major histocompatibility complex (MHC) binding affinity, the AA-associated competitor was a better inhibitor of the in vitro proliferation of arthritogenic T cells. Furthermore, although in vivo EAE was inhibited by both competitors, AA was only inhibited by the AA-associated competitor. Remarkably, in contrast to what was expected of a regular MHC competitor peptide, the AA-associated peptide analogue also prevented AA upon immunization before disease induction and appeared to induce T cell responses that crossreacted with the original disease-associated epitope. Therefore, it is concluded that antigen-specific regulatory mechanisms were involved in synergy with MHC competition. The integration of both qualities into a single "competitor-modulator" analogue peptide may lead to the development of novel, more effective, disease-specific immunomodulatory peptides.
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49

Mear, John P., Kathy L. Schreiber, Christian Münz, Xiaoming Zhu, Stefan Stevanović, Hans-Georg Rammensee, Sarah L. Rowland-Jones, and Robert A. Colbert. "Misfolding of HLA-B27 as a Result of Its B Pocket Suggests a Novel Mechanism for Its Role in Susceptibility to Spondyloarthropathies." Journal of Immunology 163, no. 12 (December 15, 1999): 6665–70. http://dx.doi.org/10.4049/jimmunol.163.12.6665.

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Abstract The MHC class I protein HLA-B27 is strongly associated with susceptibility to spondyloarthropathies and can cause arthritis when expressed in rats and mice, implying a direct role in disease pathogenesis. A prominent hypothesis to explain this role suggests that the unique peptide binding specificity of HLA-B27 confers an ability to present arthritogenic peptides. The B pocket, a region of the peptide binding groove that is an important determinant of allele-specific peptide binding, is thought to be critical for arthritogenicity. However, this hypothesis remains unproven. We show that in addition to its role in peptide selection, the B pocket causes a portion of the pool of assembling HLA-B27 heavy chains in the endoplasmic reticulum to misfold, resulting in their degradation in the cytosol. The misfolding phenotype is corrected by replacing the HLA-B27 B pocket with one from HLA-A2. Our results suggest an alternative to the arthritogenic peptide hypothesis. Misfolding and its consequences, rather than allele-specific peptide presentation, may underlie the strong link between the HLA-B27 B pocket and susceptibility to spondyloarthropathies.
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50

Gripenberg-Lerche, Christel, Lijuan Zhang, Päivi Ahtonen, Paavo Toivanen, and Mikael Skurnik. "Construction of Urease-Negative Mutants of Yersinia enterocolitica Serotypes O:3 and O:8: Role of Urease in Virulence and Arthritogenicity." Infection and Immunity 68, no. 2 (February 1, 2000): 942–47. http://dx.doi.org/10.1128/iai.68.2.942-947.2000.

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ABSTRACT Yersinia enterocolitica serotype O:3 and O:8 urease-negative mutants unable to express the 19-kDa β subunit of urease were constructed and tested for virulence and arthritogenicity. Our results indicate that urease is needed for full virulence in oral infections and that it is not an arthritogenic factor in the rat model.
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