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Issue published March 1, 2001 Previous issue | Next issue

  • Volume 107, Issue 5
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  • In this issue
  • Letters to the Editor
  • Perspectives
  • Commentaries
  • Research Articles
In this issue
In This Issue
John Ashkenas
John Ashkenas
Published March 1, 2001
Citation Information: J Clin Invest. 2001;107(5):531-531. https://doi.org/10.1172/JCI119921.
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In This Issue

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Abstract

Authors

John Ashkenas

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Letters to the Editor
Human C-reactive protein does not bind to fcγRIIa on phagocyti cells
Eirikur Saeland, … , Lieke A.M. Sanders, Jan G.J. van de Winkel
Eirikur Saeland, … , Lieke A.M. Sanders, Jan G.J. van de Winkel
Published March 1, 2001
Citation Information: J Clin Invest. 2001;107(5):641-642. https://doi.org/10.1172/JCI12418.
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Human C-reactive protein does not bind to fcγRIIa on phagocyti cells

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Abstract

Authors

Eirikur Saeland, Annet van Royen, Karin Hendriksen, Henriette Vilé-Weekhout, Ger T. Rijkers, Lieke A.M. Sanders, Jan G.J. van de Winkel

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Modulation of MDR/MRP by wild-type and mutant p53
Oliver Bähr, … , Wolfgang Wick, Michael Weller
Oliver Bähr, … , Wolfgang Wick, Michael Weller
Published March 1, 2001
Citation Information: J Clin Invest. 2001;107(5):643-645. https://doi.org/10.1172/JCI12415.
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Modulation of MDR/MRP by wild-type and mutant p53

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Abstract

Authors

Oliver Bähr, Wolfgang Wick, Michael Weller

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Perspectives
The nature and consequence of genetic variability within Mycobacterium tuberculosis
M. Kato-Maeda, … , B.N. Kreiswirth, P.M. Small
M. Kato-Maeda, … , B.N. Kreiswirth, P.M. Small
Published March 1, 2001
Citation Information: J Clin Invest. 2001;107(5):533-537. https://doi.org/10.1172/JCI11426.
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The nature and consequence of genetic variability within Mycobacterium tuberculosis

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Abstract

Authors

M. Kato-Maeda, P.J. Bifani, B.N. Kreiswirth, P.M. Small

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Pathogenesis and evolution of virulence in enteropathogenic and enterohemorrhagic Escherichia coli
Michael S. Donnenberg, Thomas S. Whittam
Michael S. Donnenberg, Thomas S. Whittam
Published March 1, 2001
Citation Information: J Clin Invest. 2001;107(5):539-548. https://doi.org/10.1172/JCI12404.
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Pathogenesis and evolution of virulence in enteropathogenic and enterohemorrhagic Escherichia coli

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Abstract

Authors

Michael S. Donnenberg, Thomas S. Whittam

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Commentaries
MHC class II genotype and the control of viremia in HIV-1–infected individuals on highly active antiretroviral therapy
Joel N. Blankson, Robert F. Siliciano
Joel N. Blankson, Robert F. Siliciano
Published March 1, 2001
Citation Information: J Clin Invest. 2001;107(5):549-557. https://doi.org/10.1172/JCI12430.
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MHC class II genotype and the control of viremia in HIV-1–infected individuals on highly active antiretroviral therapy

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Abstract

Authors

Joel N. Blankson, Robert F. Siliciano

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How much help does a vaccine-induced T-cell response need?
Jeffrey S. Weber, James J. Mulé
Jeffrey S. Weber, James J. Mulé
Published March 1, 2001
Citation Information: J Clin Invest. 2001;107(5):553-554. https://doi.org/10.1172/JCI12403.
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How much help does a vaccine-induced T-cell response need?

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Abstract

Authors

Jeffrey S. Weber, James J. Mulé

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Research Articles
Natural killer type 2 bias in remission of multiple sclerosis
Kazuya Takahashi, … , Shuji Hashimoto, Takashi Yamamura
Kazuya Takahashi, … , Shuji Hashimoto, Takashi Yamamura
Published March 1, 2001
Citation Information: J Clin Invest. 2001;107(5):R23-R29. https://doi.org/10.1172/JCI11819.
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Natural killer type 2 bias in remission of multiple sclerosis

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Multiple sclerosis (MS) is an autoimmune disease characterized by clinical relapse and remission. Because of the potential role of natural killer (NK) cells in the regulation of autoimmunity, we have examined cytokine profile and surface phenotype of NK cells in the peripheral blood of MS. Here we demonstrate that NK cells in the remission of MS are characterized by a remarkable elevation of IL-5 mRNA and a decreased expression of IL-12Rβ2 mRNA, as well as a higher expression of CD95. Moreover, the NK cells from MS in remission produced much larger amounts of IL-5 than did those from controls after stimulation with phorbol myristate acetate (PMA) and ionomycin. These features are reminiscent of those of NK type 2 (NK2) cells that can be induced in a condition favoring functional deviation of T cells toward Th2. Remarkably, the NK cells lose the NK2-like property when relapse of MS occurs, but regain it after recovery. We also found that NK2 cells induced in vitro inhibit induction of Th1 cells, suggesting that the NK2-like cells in vivo may also prohibit autoimmune effector T cells. Taken together, it is possible that NK cells play an active role in maintaining the remission of MS.

Authors

Kazuya Takahashi, Sachiko Miyake, Takayuki Kondo, Keiji Terao, Megumi Hatakenaka, Shuji Hashimoto, Takashi Yamamura

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Self-antigen–presenting cells expressing diabetes-associated autoantigens exist in both thymus and peripheral lymphoid organs
Alberto Pugliese, … , Dhavalkumar D. Patel, Camillo Ricordi
Alberto Pugliese, … , Dhavalkumar D. Patel, Camillo Ricordi
Published March 1, 2001
Citation Information: J Clin Invest. 2001;107(5):555-564. https://doi.org/10.1172/JCI10860.
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Self-antigen–presenting cells expressing diabetes-associated autoantigens exist in both thymus and peripheral lymphoid organs

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Recent reports indicate that genes with tissue-restricted expression, including those encoding the type 1 diabetes autoantigens insulin, glutamic acid decarboxylase (GAD), and the tyrosine-phosphatase-like protein IA-2 (or ICA512), are transcribed in the thymus. The reported modulation of diabetes susceptibility by genetically determined differences in thymic insulin levels and studies in transgenic mice provide correlative and functional evidence that thymic expression of peripheral proteins is crucial for immunological self-tolerance. However, there are no specific data about the existence, tissue distribution, phenotype, and function of those cells that express insulin and other self-antigens in the human thymus. We find that the human thymus harbors specialized cells synthesizing (pro)insulin, GAD, and IA-2, mainly localized in the medulla, and we demonstrate such cells also in peripheral lymphoid organs (spleen and lymph nodes). Phenotypic analysis qualifies these cells as antigen-presenting cells (APCs), including both dendritic cells and macrophages. These cells often appear surrounded by apoptotic lymphocytes, both in thymus and spleen, and may therefore be involved in the deletion of autoreactive lymphocytes. Our findings demonstrate the existence of, and define the tissue distribution and phenotype of, a novel subset of APCs expressing self-antigens in human lymphoid organs that appear to be involved in the regulation of self-tolerance throughout life.

Authors

Alberto Pugliese, Douglas Brown, David Garza, Djanira Murchison, Markus Zeller, Maria Redondo, Juan Diez, George S. Eisenbarth, Dhavalkumar D. Patel, Camillo Ricordi

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Hepatic cholesterol metabolism and resistance to dietary cholesterol in LXRβ-deficient mice
S. Alberti, … , S. Pettersson, J.-Å. Gustafsson
S. Alberti, … , S. Pettersson, J.-Å. Gustafsson
Published March 1, 2001
Citation Information: J Clin Invest. 2001;107(5):565-573. https://doi.org/10.1172/JCI9794.
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Hepatic cholesterol metabolism and resistance to dietary cholesterol in LXRβ-deficient mice

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The nuclear oxysterol-receptor paralogues LXRα and LXRβ share a high degree of amino acid identity and bind endogenous oxysterol ligands with similar affinities. While LXRα has been established as an important regulator of cholesterol catabolism in cholesterol-fed mice, little is known about the function of LXRβ in vivo. We have generated mouse lines with targeted disruptions of each of these LXR receptors and have compared their responses to dietary cholesterol. Serum and hepatic cholesterol levels and lipoprotein profiles of cholesterol-fed animals revealed no significant differences between LXRβ–/– and wild-type mice. Steady-state mRNA levels of 3-hydroxy-3-methylglutaryl coenzyme A reductase, farnesyl diphosphate synthase, and squalene synthase were increased in LXRβ–/– mice compared with LXRβ+/+ mice, when fed standard chow. The mRNA levels for cholesterol 7α-hydroxylase, oxysterol 7α-hydroxylase, sterol 12α-hydroxylase, and sterol 27-hydroxylase, respectively, were comparable in these strains, both on standard and 2% cholesterol chow. Our results indicate that LXRβ–/– mice — in contrast to LXRα–/– mice — maintain their resistance to dietary cholesterol, despite subtle effects on the expression of genes coding for enzymes involved in lipid metabolism. Thus, our data indicate that LXRβ has no complete overlapping function compared with LXRα in the liver.

Authors

S. Alberti, G. Schuster, P. Parini, D. Feltkamp, U. Diczfalusy, M. Rudling, B. Angelin, I. Björkhem, S. Pettersson, J.-Å. Gustafsson

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CD28-independent induction of experimental autoimmune encephalomyelitis
Tanuja Chitnis, … , Mohamed H. Sayegh, Samia J. Khoury
Tanuja Chitnis, … , Mohamed H. Sayegh, Samia J. Khoury
Published March 1, 2001
Citation Information: J Clin Invest. 2001;107(5):575-583. https://doi.org/10.1172/JCI11220.
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CD28-independent induction of experimental autoimmune encephalomyelitis

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Experimental autoimmune encephalomyelitis (EAE) is a T cell–mediated disease initiated by antigen-specific CD4+ T cells. Signaling through CD28 is a critical second signal for activation of T cells, and CD28 knockout (CD28KO) mice have been reported to be resistant to induction of EAE. We now report that CD28KO mice have no intrinsic defect in mediating disease, because they developed EAE after passive transfer of primed T cells. After immunization, peripheral T cells from CD28KO mice were primed and developed memory phenotype, but had decreased antigen-specific IFN-γ production as compared with cells from wild-type (WT) animals. Reimmunization of CD28KO mice brought out clinical disease and increased IFN-γ production in vitro. Pathologically, there were cellular infiltrates in the central nervous system, in contrast to single-immunized mice. We show furthermore that blocking B7-1 or CTLA4, but not B7-2, in CD28KO mice induces disease after a single immunization. Thus, EAE can be induced in animals lacking CD28-dependent costimulation, suggesting that alternative costimulatory pathways were used. Blocking the OX40-OX40L costimulatory pathway differentially affected disease induction in CD28KO mice as compared with WT controls. Our data show that EAE may develop in the absence of CD28 T-cell costimulation. These findings have implications for therapies aimed at blocking costimulatory signals in autoimmune diseases.

Authors

Tanuja Chitnis, Nader Najafian, Kald A. Abdallah, Victor Dong, Hideo Yagita, Mohamed H. Sayegh, Samia J. Khoury

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Increased sensitivity to dextran sodium sulfate colitis in IRE1β-deficient mice
Anne Bertolotti, … , A. Brian West, David Ron
Anne Bertolotti, … , A. Brian West, David Ron
Published March 1, 2001
Citation Information: J Clin Invest. 2001;107(5):585-593. https://doi.org/10.1172/JCI11476.
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Increased sensitivity to dextran sodium sulfate colitis in IRE1β-deficient mice

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The epithelial cells of the gastrointestinal tract are exposed to toxins and infectious agents that can adversely affect protein folding in the endoplasmic reticulum (ER) and cause ER stress. The IRE1 genes are implicated in sensing and responding to ER stress signals. We found that epithelial cells of the gastrointestinal tract express IRE1β, a specific isoform of IRE1. BiP protein, a marker of ER stress, was elevated in the colonic mucosa of IRE1β–/– mice, and, when exposed to dextran sodium sulfate (DSS) to induce inflammatory bowel disease, mutant mice developed colitis 3–5 days earlier than did wild-type or IRE1β+/– mice. The inflammation marker ICAM-1 was also expressed earlier in the colonic mucosa of DSS-treated IRE1β–/– mice, indicating that the mutation had its impact early in the inflammatory process, before the onset of mucosal ulceration. These findings are consistent with a model whereby perturbations in ER function, which are normally mitigated by the activity of IRE1β, participate in the development of colitis.

Authors

Anne Bertolotti, XiaoZhong Wang, Isabel Novoa, Rivka Jungreis, Karni Schlessinger, Judy H. Cho, A. Brian West, David Ron

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Bonzo/CXCR6 expression defines type 1–polarized T-cell subsets with extralymphoid tissue homing potential
Chang H. Kim, … , Harry B. Greenberg, Eugene C. Butcher
Chang H. Kim, … , Harry B. Greenberg, Eugene C. Butcher
Published March 1, 2001
Citation Information: J Clin Invest. 2001;107(5):595-601. https://doi.org/10.1172/JCI11902.
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Bonzo/CXCR6 expression defines type 1–polarized T-cell subsets with extralymphoid tissue homing potential

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Chemokine receptor expression is finely controlled during T-cell development. We show that newly identified chemokine receptor Bonzo/CXCR6 is expressed by subsets of Th1 or T-cytotoxic 1 (Tc1) cells, but not by Th2 or Tc2 cells, establishing Bonzo as a differential marker of polarized type 1 T cells in vitro and in vivo. Priming of naive T cells by dendritic cells induces expression of Bonzo on T cells. IL-12 enhances this dendritic cell–dependent upregulation, while IL-4 inhibits it. In blood, 35–56% of Bonzo+ CD4 T cells are Th1 cells, and 60–65% of Bonzo+ CD8 T cells are Tc1 cells, while few Bonzo+ cells are type 2 T cells. Almost all Bonzo+ Tc1 cells contain preformed granzyme A and display cytotoxic effector phenotype. Most Bonzo+ T cells lack L-selectin and/or CCR7, homing receptors for lymphoid tissues. Instead, Bonzo+ T cells are dramatically enriched among T cells in tissue sites of inflammation, such as rheumatoid joints and inflamed livers. Bonzo may be important in trafficking of effector T cells that mediate type 1 inflammation, making it a potential target for therapeutic modulation of inflammatory diseases.

Authors

Chang H. Kim, Eric J. Kunkel, Judie Boisvert, Brent Johnston, James J. Campbell, Mark C. Genovese, Harry B. Greenberg, Eugene C. Butcher

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Activation of the murine EP3 receptor for PGE2 inhibits cAMP production and promotes platelet aggregation
Jean-Etienne Fabre, … , Thomas M. Coffman, Beverly H. Koller
Jean-Etienne Fabre, … , Thomas M. Coffman, Beverly H. Koller
Published March 1, 2001
Citation Information: J Clin Invest. 2001;107(5):603-610. https://doi.org/10.1172/JCI10881.
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Activation of the murine EP3 receptor for PGE2 inhibits cAMP production and promotes platelet aggregation

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The importance of arachidonic acid metabolites (termed eicosanoids), particularly those derived from the COX-1 and COX-2 pathways (termed prostanoids), in platelet homeostasis has long been recognized. Thromboxane is a potent agonist, whereas prostacyclin is an inhibitor of platelet aggregation. In contrast, the effect of prostaglandin E2 (PGE2) on platelet aggregation varies significantly depending on its concentration. Low concentrations of PGE2 enhance platelet aggregation, whereas high PGE2 levels inhibit aggregation. The mechanism for this dual action of PGE2 is not clear. This study shows that among the four PGE2 receptors (EP1–EP4), activation of EP3 is sufficient to mediate the proaggregatory actions of low PGE2 concentration. In contrast, the prostacyclin receptor (IP) mediates the inhibitory effect of higher PGE2 concentrations. Furthermore, the relative activation of these two receptors, EP3 and IP, regulates the intracellular level of cAMP and in this way conditions the response of the platelet to aggregating agents. Consistent with these findings, loss of the EP3 receptor in a model of venous inflammation protects against formation of intravascular clots. Our results suggest that local production of PGE2 during an inflammatory process can modulate ensuing platelet responses.

Authors

Jean-Etienne Fabre, MyTrang Nguyen, Krairek Athirakul, Kenneth Coggins, John D. McNeish, Sandra Austin, Leslie K. Parise, Garret A. FitzGerald, Thomas M. Coffman, Beverly H. Koller

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Helicobacter pylori strain-specific differences in genetic content, identified by microarray, influence host inflammatory responses
Dawn A. Israel, … , Stanley Falkow, Richard M. Peek Jr.
Dawn A. Israel, … , Stanley Falkow, Richard M. Peek Jr.
Published March 1, 2001
Citation Information: J Clin Invest. 2001;107(5):611-620. https://doi.org/10.1172/JCI11450.
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Helicobacter pylori strain-specific differences in genetic content, identified by microarray, influence host inflammatory responses

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Abstract

Helicobacter pylori enhances the risk for ulcer disease and gastric cancer, yet only a minority of H. pylori–colonized individuals develop disease. We examined the ability of two H. pylori isolates to induce differential host responses in vivo or in vitro, and then used an H. pylori whole genome microarray to identify bacterial determinants related to pathogenesis. Gastric ulcer strain B128 induced more severe gastritis, proliferation, and apoptosis in gerbil mucosa than did duodenal ulcer strain G1.1, and gastric ulceration and atrophy occurred only in B128+ gerbils. In vitro, gerbil-passaged B128 derivatives significantly increased IL-8 secretion and apoptosis compared with G1.1 strains. DNA hybridization to the microarray identified several strain-specific differences in gene composition including a large deletion of the cag pathogenicity island in strain G1.1. Partial and complete disruption of the cag island in strain B128 attenuated induction of IL-8 in vitro and significantly decreased gastric inflammation in vivo. These results indicate that the ability of H. pylori to regulate epithelial cell responses related to inflammation depends on the presence of an intact cag pathogenicity island. Use of an H. pylori whole genome microarray is an effective method to identify differences in gene content between H. pylori strains that induce distinct pathological outcomes in a rodent model of H. pylori infection.

Authors

Dawn A. Israel, Nina Salama, Carrie N. Arnold, Steven F. Moss, Takafumi Ando, Hans-Peter Wirth, Kyi T. Tham, Margorita Camorlinga, Martin J. Blaser, Stanley Falkow, Richard M. Peek Jr.

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Translocated EspF protein from enteropathogenic Escherichia coli disrupts host intestinal barrier function
Barry P. McNamara, … , Michael S. Donnenberg, Gail Hecht
Barry P. McNamara, … , Michael S. Donnenberg, Gail Hecht
Published March 1, 2001
Citation Information: J Clin Invest. 2001;107(5):621-629. https://doi.org/10.1172/JCI11138.
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Translocated EspF protein from enteropathogenic Escherichia coli disrupts host intestinal barrier function

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Abstract

The mechanisms by which enteropathogenic Escherichia coli (EPEC), an important cause of diarrhea among infants in developing countries, induce symptoms are not defined. EPEC have a type III secretion system required for characteristic attaching and effacing changes that modify the cytoskeleton and apical surface of host cells. Infection of polarized intestinal epithelial cell monolayers by EPEC leads to a loss of transepithelial electrical resistance, which also requires the type III secretion system. We demonstrate here that EspF, a protein that is secreted by EPEC via the type III secretion system, is not required for quantitatively and qualitatively typical attaching and effacing lesion formation in intestinal epithelial cells. However, EspF is required in a dose-dependent fashion for the loss of transepithelial electrical resistance, for increased monolayer permeability, and for redistribution of the tight junction–associated protein occludin. Furthermore, the analysis of EPEC strains expressing EspF-adenylate cyclase fusion proteins indicates that EspF is translocated via the type III secretion system to the cytoplasm of host cells, a result confirmed by immunofluorescence microscopy. These studies suggest a novel role for EspF as an effector protein that disrupts intestinal barrier function without involvement in attaching and effacing lesion formation.

Authors

Barry P. McNamara, Athanasia Koutsouris, Colin B. O’Connell, Jean-Philippe Nougayréde, Michael S. Donnenberg, Gail Hecht

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Amelioration of collagen-induced arthritis by thrombin inhibition
Ingrid Marty, … , Alexander So, Nathalie Busso
Ingrid Marty, … , Alexander So, Nathalie Busso
Published March 1, 2001
Citation Information: J Clin Invest. 2001;107(5):631-640. https://doi.org/10.1172/JCI11064.
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Amelioration of collagen-induced arthritis by thrombin inhibition

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The deleterious role of fibrin deposition in arthritic joints prompted us to explore the effect of the thrombin inhibition on the course of collagen-induced arthritis (CIA) in the mouse. CIA was induced in male DBA/1J mice using native chicken type II collagen. The thrombin inhibitor polyethyleneglycol-hirudin (PEG-hirudin) was given for 16 days, starting 20 days after the first immunization (preventive treatment) or at the onset of clinical signs of arthritis (curative treatment). All the mice treated with PEG-hirudin had a significantly prolonged clotting time compared with control mice. PEG-hirudin, administered in a preventive way, led to significantly reduced incidence and severity of CIA during most of the treatment period, as assessed by clinical scoring. Accordingly, histological features showed a significant diminution of synovial hyperplasia in PEG-hirudin–treated mice compared with untreated mice. There was also a significant downmodulation of the synovial proinflammatory IL-1β and IL-12p35 cytokine mRNAs in treated mice. Intra-articular fibrin, evaluated by immunohistochemistry, was significantly reduced in treated mice compared with control mice and correlated with both clinical and histological scorings. Most importantly, once arthritis was established, PEG-hirudin also showed a curative effect. In conclusion, PEG-hirudin can both prevent the onset of CIA in a dose-dependent manner and ameliorate established arthritis, suggesting that thrombin inhibition may offer a new therapeutic approach in arthritis.

Authors

Ingrid Marty, Veronique Péclat, Gailute Kirdaite, Roberto Salvi, Alexander So, Nathalie Busso

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