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1. Transancestral mapping and genetic load in systemic lupus erythematosus.

Author

Langefeld, Carl D, Langefeld, Carl D, Ainsworth, Hannah C, Cunninghame Graham, Deborah S, Kelly, Jennifer A, Comeau, Mary E, Marion, Miranda C, Howard, Timothy D, Ramos, Paula S, Croker, Jennifer A, Morris, David L, Sandling, Johanna K, Almlöf, Jonas Carlsson, Acevedo-Vásquez, Eduardo M, Alarcón, Graciela S, Babini, Alejandra M, Baca, Vicente, Bengtsson, Anders A, Berbotto, Guillermo A, Bijl, Marc, Brown, Elizabeth E, Brunner, Hermine I, Cardiel, Mario H, Catoggio, Luis, Cervera, Ricard, Cucho-Venegas, Jorge M, Dahlqvist, Solbritt Rantapää, D'Alfonso, Sandra, Da Silva, Berta Martins, de la Rúa Figueroa, Iñigo, Doria, Andrea, Edberg, Jeffrey C, Endreffy, Emőke, Esquivel-Valerio, Jorge A, Fortin, Paul R, Freedman, Barry I, Frostegård, Johan, García, Mercedes A, de la Torre, Ignacio García, Gilkeson, Gary S, Gladman, Dafna D, Gunnarsson, Iva, Guthridge, Joel M, Huggins, Jennifer L, James, Judith A, Kallenberg, Cees GM, Kamen, Diane L, Karp, David R, Kaufman, Kenneth M, Kottyan, Leah C, Kovács, László, Laustrup, Helle, Lauwerys, Bernard R, Li, Quan-Zhen, Maradiaga-Ceceña, Marco A, Martín, Javier, McCune, Joseph M, McWilliams, David R, Merrill, Joan T, Miranda, Pedro, Moctezuma, José F, Nath, Swapan K, Niewold, Timothy B, Orozco, Lorena, Ortego-Centeno, Norberto, Petri, Michelle, Pineau, Christian A, Pons-Estel, Bernardo A, Pope, Janet, Raj, Prithvi, Ramsey-Goldman, Rosalind, Reveille, John D, Russell, Laurie P, Sabio, José M, Aguilar-Salinas, Carlos A, Scherbarth, Hugo R, Scorza, Raffaella, Seldin, Michael F, Sjöwall, Christopher, Svenungsson, Elisabet, Thompson, Susan D, Toloza, Sergio MA, Truedsson, Lennart, Tusié-Luna, Teresa, Vasconcelos, Carlos, Vilá, Luis M, Wallace, Daniel J, Weisman, Michael H, Wither, Joan E, Bhangale, Tushar, Oksenberg, Jorge R, Rioux, John D, Gregersen, Peter K, Syvänen, Ann-Christine, Rönnblom, Lars, Criswell, Lindsey A, Jacob, Chaim O, Sivils, Kathy L, Tsao, Betty P, Schanberg, Laura E, Behrens, Timothy W, Langefeld, Carl D, Langefeld, Carl D, Ainsworth, Hannah C, Cunninghame Graham, Deborah S, Kelly, Jennifer A, Comeau, Mary E, Marion, Miranda C, Howard, Timothy D, Ramos, Paula S, Croker, Jennifer A, Morris, David L, Sandling, Johanna K, Almlöf, Jonas Carlsson, Acevedo-Vásquez, Eduardo M, Alarcón, Graciela S, Babini, Alejandra M, Baca, Vicente, Bengtsson, Anders A, Berbotto, Guillermo A, Bijl, Marc, Brown, Elizabeth E, Brunner, Hermine I, Cardiel, Mario H, Catoggio, Luis, Cervera, Ricard, Cucho-Venegas, Jorge M, Dahlqvist, Solbritt Rantapää, D'Alfonso, Sandra, Da Silva, Berta Martins, de la Rúa Figueroa, Iñigo, Doria, Andrea, Edberg, Jeffrey C, Endreffy, Emőke, Esquivel-Valerio, Jorge A, Fortin, Paul R, Freedman, Barry I, Frostegård, Johan, García, Mercedes A, de la Torre, Ignacio García, Gilkeson, Gary S, Gladman, Dafna D, Gunnarsson, Iva, Guthridge, Joel M, Huggins, Jennifer L, James, Judith A, Kallenberg, Cees GM, Kamen, Diane L, Karp, David R, Kaufman, Kenneth M, Kottyan, Leah C, Kovács, László, Laustrup, Helle, Lauwerys, Bernard R, Li, Quan-Zhen, Maradiaga-Ceceña, Marco A, Martín, Javier, McCune, Joseph M, McWilliams, David R, Merrill, Joan T, Miranda, Pedro, Moctezuma, José F, Nath, Swapan K, Niewold, Timothy B, Orozco, Lorena, Ortego-Centeno, Norberto, Petri, Michelle, Pineau, Christian A, Pons-Estel, Bernardo A, Pope, Janet, Raj, Prithvi, Ramsey-Goldman, Rosalind, Reveille, John D, Russell, Laurie P, Sabio, José M, Aguilar-Salinas, Carlos A, Scherbarth, Hugo R, Scorza, Raffaella, Seldin, Michael F, Sjöwall, Christopher, Svenungsson, Elisabet, Thompson, Susan D, Toloza, Sergio MA, Truedsson, Lennart, Tusié-Luna, Teresa, Vasconcelos, Carlos, Vilá, Luis M, Wallace, Daniel J, Weisman, Michael H, Wither, Joan E, Bhangale, Tushar, Oksenberg, Jorge R, Rioux, John D, Gregersen, Peter K, Syvänen, Ann-Christine, Rönnblom, Lars, Criswell, Lindsey A, Jacob, Chaim O, Sivils, Kathy L, Tsao, Betty P, Schanberg, Laura E, and Behrens, Timothy W

Abstract

Systemic lupus erythematosus (SLE) is an autoimmune disease with marked gender and ethnic disparities. We report a large transancestral association study of SLE using Immunochip genotype data from 27,574 individuals of European (EA), African (AA) and Hispanic Amerindian (HA) ancestry. We identify 58 distinct non-HLA regions in EA, 9 in AA and 16 in HA (∼50% of these regions have multiple independent associations); these include 24 novel SLE regions (P<5 × 10-8), refined association signals in established regions, extended associations to additional ancestries, and a disentangled complex HLA multigenic effect. The risk allele count (genetic load) exhibits an accelerating pattern of SLE risk, leading us to posit a cumulative hit hypothesis for autoimmune disease. Comparing results across the three ancestries identifies both ancestry-dependent and ancestry-independent contributions to SLE risk. Our results are consistent with the unique and complex histories of the populations sampled, and collectively help clarify the genetic architecture and ethnic disparities in SLE.

Published
2017

2. Transancestral mapping and genetic load in systemic lupus erythematosus.

Author

Langefeld, Carl D, Langefeld, Carl D, Ainsworth, Hannah C, Cunninghame Graham, Deborah S, Kelly, Jennifer A, Comeau, Mary E, Marion, Miranda C, Howard, Timothy D, Ramos, Paula S, Croker, Jennifer A, Morris, David L, Sandling, Johanna K, Almlöf, Jonas Carlsson, Acevedo-Vásquez, Eduardo M, Alarcón, Graciela S, Babini, Alejandra M, Baca, Vicente, Bengtsson, Anders A, Berbotto, Guillermo A, Bijl, Marc, Brown, Elizabeth E, Brunner, Hermine I, Cardiel, Mario H, Catoggio, Luis, Cervera, Ricard, Cucho-Venegas, Jorge M, Dahlqvist, Solbritt Rantapää, D'Alfonso, Sandra, Da Silva, Berta Martins, de la Rúa Figueroa, Iñigo, Doria, Andrea, Edberg, Jeffrey C, Endreffy, Emőke, Esquivel-Valerio, Jorge A, Fortin, Paul R, Freedman, Barry I, Frostegård, Johan, García, Mercedes A, de la Torre, Ignacio García, Gilkeson, Gary S, Gladman, Dafna D, Gunnarsson, Iva, Guthridge, Joel M, Huggins, Jennifer L, James, Judith A, Kallenberg, Cees GM, Kamen, Diane L, Karp, David R, Kaufman, Kenneth M, Kottyan, Leah C, Kovács, László, Laustrup, Helle, Lauwerys, Bernard R, Li, Quan-Zhen, Maradiaga-Ceceña, Marco A, Martín, Javier, McCune, Joseph M, McWilliams, David R, Merrill, Joan T, Miranda, Pedro, Moctezuma, José F, Nath, Swapan K, Niewold, Timothy B, Orozco, Lorena, Ortego-Centeno, Norberto, Petri, Michelle, Pineau, Christian A, Pons-Estel, Bernardo A, Pope, Janet, Raj, Prithvi, Ramsey-Goldman, Rosalind, Reveille, John D, Russell, Laurie P, Sabio, José M, Aguilar-Salinas, Carlos A, Scherbarth, Hugo R, Scorza, Raffaella, Seldin, Michael F, Sjöwall, Christopher, Svenungsson, Elisabet, Thompson, Susan D, Toloza, Sergio MA, Truedsson, Lennart, Tusié-Luna, Teresa, Vasconcelos, Carlos, Vilá, Luis M, Wallace, Daniel J, Weisman, Michael H, Wither, Joan E, Bhangale, Tushar, Oksenberg, Jorge R, Rioux, John D, Gregersen, Peter K, Syvänen, Ann-Christine, Rönnblom, Lars, Criswell, Lindsey A, Jacob, Chaim O, Sivils, Kathy L, Tsao, Betty P, Schanberg, Laura E, Behrens, Timothy W, Langefeld, Carl D, Langefeld, Carl D, Ainsworth, Hannah C, Cunninghame Graham, Deborah S, Kelly, Jennifer A, Comeau, Mary E, Marion, Miranda C, Howard, Timothy D, Ramos, Paula S, Croker, Jennifer A, Morris, David L, Sandling, Johanna K, Almlöf, Jonas Carlsson, Acevedo-Vásquez, Eduardo M, Alarcón, Graciela S, Babini, Alejandra M, Baca, Vicente, Bengtsson, Anders A, Berbotto, Guillermo A, Bijl, Marc, Brown, Elizabeth E, Brunner, Hermine I, Cardiel, Mario H, Catoggio, Luis, Cervera, Ricard, Cucho-Venegas, Jorge M, Dahlqvist, Solbritt Rantapää, D'Alfonso, Sandra, Da Silva, Berta Martins, de la Rúa Figueroa, Iñigo, Doria, Andrea, Edberg, Jeffrey C, Endreffy, Emőke, Esquivel-Valerio, Jorge A, Fortin, Paul R, Freedman, Barry I, Frostegård, Johan, García, Mercedes A, de la Torre, Ignacio García, Gilkeson, Gary S, Gladman, Dafna D, Gunnarsson, Iva, Guthridge, Joel M, Huggins, Jennifer L, James, Judith A, Kallenberg, Cees GM, Kamen, Diane L, Karp, David R, Kaufman, Kenneth M, Kottyan, Leah C, Kovács, László, Laustrup, Helle, Lauwerys, Bernard R, Li, Quan-Zhen, Maradiaga-Ceceña, Marco A, Martín, Javier, McCune, Joseph M, McWilliams, David R, Merrill, Joan T, Miranda, Pedro, Moctezuma, José F, Nath, Swapan K, Niewold, Timothy B, Orozco, Lorena, Ortego-Centeno, Norberto, Petri, Michelle, Pineau, Christian A, Pons-Estel, Bernardo A, Pope, Janet, Raj, Prithvi, Ramsey-Goldman, Rosalind, Reveille, John D, Russell, Laurie P, Sabio, José M, Aguilar-Salinas, Carlos A, Scherbarth, Hugo R, Scorza, Raffaella, Seldin, Michael F, Sjöwall, Christopher, Svenungsson, Elisabet, Thompson, Susan D, Toloza, Sergio MA, Truedsson, Lennart, Tusié-Luna, Teresa, Vasconcelos, Carlos, Vilá, Luis M, Wallace, Daniel J, Weisman, Michael H, Wither, Joan E, Bhangale, Tushar, Oksenberg, Jorge R, Rioux, John D, Gregersen, Peter K, Syvänen, Ann-Christine, Rönnblom, Lars, Criswell, Lindsey A, Jacob, Chaim O, Sivils, Kathy L, Tsao, Betty P, Schanberg, Laura E, and Behrens, Timothy W

Abstract

Systemic lupus erythematosus (SLE) is an autoimmune disease with marked gender and ethnic disparities. We report a large transancestral association study of SLE using Immunochip genotype data from 27,574 individuals of European (EA), African (AA) and Hispanic Amerindian (HA) ancestry. We identify 58 distinct non-HLA regions in EA, 9 in AA and 16 in HA (∼50% of these regions have multiple independent associations); these include 24 novel SLE regions (P<5 × 10-8), refined association signals in established regions, extended associations to additional ancestries, and a disentangled complex HLA multigenic effect. The risk allele count (genetic load) exhibits an accelerating pattern of SLE risk, leading us to posit a cumulative hit hypothesis for autoimmune disease. Comparing results across the three ancestries identifies both ancestry-dependent and ancestry-independent contributions to SLE risk. Our results are consistent with the unique and complex histories of the populations sampled, and collectively help clarify the genetic architecture and ethnic disparities in SLE.

Published
2017

3. Systems analysis of primary Sjogren's syndrome pathogenesis in salivary glands identifies shared pathways in human and a mouse model

Author

Horvath, Steve, Horvath, Steve, Nazmul-Hossain, Abu NM, Pollard, Rodney PE, Kroese, Frans GM, Vissink, Arjan, Kallenberg, Cees GM, Spijkervet, Fred KL, Bootsma, Hendrika, Michie, Sara A, Gorr, Sven U, Peck, Ammon B, Cai, Chaochao, Zhou, Hui, Wong, David TW, Horvath, Steve, Horvath, Steve, Nazmul-Hossain, Abu NM, Pollard, Rodney PE, Kroese, Frans GM, Vissink, Arjan, Kallenberg, Cees GM, Spijkervet, Fred KL, Bootsma, Hendrika, Michie, Sara A, Gorr, Sven U, Peck, Ammon B, Cai, Chaochao, Zhou, Hui, and Wong, David TW

Abstract

Introduction Primary Sjögren's syndrome (pSS) is a chronic autoimmune disease with complex etiopathogenesis. Despite extensive studies to understand the disease process utilizing human and mouse models, the intersection between these species remains elusive. To address this gap, we utilized a novel systems biology approach to identify disease-related gene modules and signaling pathways that overlap between humans and mice. Methods Parotid gland tissues were harvested from 24 pSS and 16 non-pSS sicca patients and 25 controls. For mouse studies, salivary glands were harvested from C57BL/6.NOD-Aec1Aec2 mice at various times during development of pSS-like disease. RNA was analyzed with Affymetrix HG U133+2.0 arrays for human samples and with MOE430+2.0 arrays for mouse samples. The images were processed with Affymetrix software. Weighted-gene co-expression network analysis was used to identify disease-related and functional pathways. Results Nineteen co-expression modules were identified in human parotid tissue, of which four were significantly upregulated and three were downregulated in pSS patients compared with non-pSS sicca patients and controls. Notably, one of the human disease-related modules was highly preserved in the mouse model, and was enriched with genes involved in immune and inflammatory responses. Further comparison between these two species led to the identification of genes associated with leukocyte recruitment and germinal center formation. Conclusion Our systems biology analysis of genome-wide expression data from salivary gland tissue of pSS patients and from a pSS mouse model identified common dysregulated biological pathways and molecular targets underlying critical molecular alterations in pSS pathogenesis.

Published
2012

4. Systems analysis of primary Sjogren's syndrome pathogenesis in salivary glands identifies shared pathways in human and a mouse model

Author

Horvath, Steve, Horvath, Steve, Nazmul-Hossain, Abu NM, Pollard, Rodney PE, Kroese, Frans GM, Vissink, Arjan, Kallenberg, Cees GM, Spijkervet, Fred KL, Bootsma, Hendrika, Michie, Sara A, Gorr, Sven U, Peck, Ammon B, Cai, Chaochao, Zhou, Hui, Wong, David TW, Horvath, Steve, Horvath, Steve, Nazmul-Hossain, Abu NM, Pollard, Rodney PE, Kroese, Frans GM, Vissink, Arjan, Kallenberg, Cees GM, Spijkervet, Fred KL, Bootsma, Hendrika, Michie, Sara A, Gorr, Sven U, Peck, Ammon B, Cai, Chaochao, Zhou, Hui, and Wong, David TW

Abstract

Introduction Primary Sjögren's syndrome (pSS) is a chronic autoimmune disease with complex etiopathogenesis. Despite extensive studies to understand the disease process utilizing human and mouse models, the intersection between these species remains elusive. To address this gap, we utilized a novel systems biology approach to identify disease-related gene modules and signaling pathways that overlap between humans and mice. Methods Parotid gland tissues were harvested from 24 pSS and 16 non-pSS sicca patients and 25 controls. For mouse studies, salivary glands were harvested from C57BL/6.NOD-Aec1Aec2 mice at various times during development of pSS-like disease. RNA was analyzed with Affymetrix HG U133+2.0 arrays for human samples and with MOE430+2.0 arrays for mouse samples. The images were processed with Affymetrix software. Weighted-gene co-expression network analysis was used to identify disease-related and functional pathways. Results Nineteen co-expression modules were identified in human parotid tissue, of which four were significantly upregulated and three were downregulated in pSS patients compared with non-pSS sicca patients and controls. Notably, one of the human disease-related modules was highly preserved in the mouse model, and was enriched with genes involved in immune and inflammatory responses. Further comparison between these two species led to the identification of genes associated with leukocyte recruitment and germinal center formation. Conclusion Our systems biology analysis of genome-wide expression data from salivary gland tissue of pSS patients and from a pSS mouse model identified common dysregulated biological pathways and molecular targets underlying critical molecular alterations in pSS pathogenesis.

Published
2012

5. Native and recombinant proteins to analyze auto-antibodies to myeloperoxidase in pauci-immune crescentic glomerulonephritis

Author

Boomsma, Maarten M.M., Stegeman, Coen C.A., Oost-Kort, Wia W.W., Kallenberg, Cees Gm, Moguilevsky, Nicole, Limburg, Pieter P.C., Cohen Tervaert, Jan J.W., Boomsma, Maarten M.M., Stegeman, Coen C.A., Oost-Kort, Wia W.W., Kallenberg, Cees Gm, Moguilevsky, Nicole, Limburg, Pieter P.C., and Cohen Tervaert, Jan J.W.

Abstract

The prevalence of Anti-Neutrophil Cytoplasmic Antibodies (ANCA) directed against myeloperoxidase (MPO) in pauci-immune necrotizing crescentic glomerulonephritis (NCGN) is dependent on the assay(s) used. We investigated the frequency of MPO-ANCA as detected by different assays for MPO-ANCA in a large cohort of patients with biopsy-proven pauci-immune NCGN. Sera from 121 consecutive untreated patients presenting with pauci-immune NCGN were tested for ANCA directed to proteinase-3 (PR3) at diagnosis. PR3-ANCA negative sera were tested by direct ELISA using recombinant or native MPO and by capture ELISA using two different specific monoclonal antibodies directed to MPO and three different antigenic sources. Sera from 80 relevant disease controls were tested to explore the specificity of the different assays. Thirty-eight out of 121 patients (31%) with pauci-immune NCGN did not have PR3-ANCA. Sufficient amounts of serum from 30 of these 38 PR3-ANCA negative patients were available for further testing. Recombinant and native MPO were recognized by similar numbers of sera in a direct ELISA (recombinant MPO: 93%, native MPO: 93%) and a capture ELISA (recombinant MPO: 77-87%, native MPO: 93%). Sera of patients with PR3-ANCA positive pauci-immune NCGN and disease controls were less frequently positive for MPO-ANCA in a capture ELISA (recombinant MPO: 3-7%, native MPO: 6-7%) than in a direct ELISA (recombinant MPO: 25%, native MPO: 13%). Both direct and capture ELISA assays using either native or recombinant MPO are sensitive techniques to detect MPO-ANCA in patients with pauci-immune NCGN. A capture ELISA performs better than a direct ELISA because it combines a higher specificity with a comparable sensitivity. Recombinant MPO is a good alternative for native MPO when used as antigen in a capture ELISA, but not when used in a direct ELISA because of lower specificity in this latter assay. © 2001 Elsevier Science B.V., SCOPUS: ar.j, info:eu-repo/semantics/published

Published
2001

6. Native and recombinant proteins to analyze auto-antibodies to myeloperoxidase in pauci-immune crescentic glomerulonephritis

Author

Boomsma, Maarten M.M., Stegeman, Coen C.A., Oost-Kort, Wia W.W., Kallenberg, Cees Gm, Moguilevsky, Nicole, Limburg, Pieter P.C., Cohen Tervaert, Jan J.W., Boomsma, Maarten M.M., Stegeman, Coen C.A., Oost-Kort, Wia W.W., Kallenberg, Cees Gm, Moguilevsky, Nicole, Limburg, Pieter P.C., and Cohen Tervaert, Jan J.W.

Abstract

The prevalence of Anti-Neutrophil Cytoplasmic Antibodies (ANCA) directed against myeloperoxidase (MPO) in pauci-immune necrotizing crescentic glomerulonephritis (NCGN) is dependent on the assay(s) used. We investigated the frequency of MPO-ANCA as detected by different assays for MPO-ANCA in a large cohort of patients with biopsy-proven pauci-immune NCGN. Sera from 121 consecutive untreated patients presenting with pauci-immune NCGN were tested for ANCA directed to proteinase-3 (PR3) at diagnosis. PR3-ANCA negative sera were tested by direct ELISA using recombinant or native MPO and by capture ELISA using two different specific monoclonal antibodies directed to MPO and three different antigenic sources. Sera from 80 relevant disease controls were tested to explore the specificity of the different assays. Thirty-eight out of 121 patients (31%) with pauci-immune NCGN did not have PR3-ANCA. Sufficient amounts of serum from 30 of these 38 PR3-ANCA negative patients were available for further testing. Recombinant and native MPO were recognized by similar numbers of sera in a direct ELISA (recombinant MPO: 93%, native MPO: 93%) and a capture ELISA (recombinant MPO: 77-87%, native MPO: 93%). Sera of patients with PR3-ANCA positive pauci-immune NCGN and disease controls were less frequently positive for MPO-ANCA in a capture ELISA (recombinant MPO: 3-7%, native MPO: 6-7%) than in a direct ELISA (recombinant MPO: 25%, native MPO: 13%). Both direct and capture ELISA assays using either native or recombinant MPO are sensitive techniques to detect MPO-ANCA in patients with pauci-immune NCGN. A capture ELISA performs better than a direct ELISA because it combines a higher specificity with a comparable sensitivity. Recombinant MPO is a good alternative for native MPO when used as antigen in a capture ELISA, but not when used in a direct ELISA because of lower specificity in this latter assay. © 2001 Elsevier Science B.V., SCOPUS: ar.j, info:eu-repo/semantics/published

Published
2001

7. Development and standardization of solid phase assays for the detection of anti-neutrophil cytoplasmic antibodies (ANCA). A report on the second phase of an international cooperative study on the standardization of ANCA assays

Author

Hagen, Ernst Christiaan, Andrassy, Konrad, Csernok, Elena, Daha, Mohamed, Gaskin, Gill, Gross, W.L., Hansen, Bettina, Heigl, Z., Hermans, Julie, Jayne, David R.W.David, Kallenberg, Cees Gm, Lesavre, Philippe, Lockwood, Christopher Martin, Lüdemann, J., Mascart, Françoise, Mirapeix, Eduardo, Pusey, Charles Dickson, Rasmussen, Niels, Sinico, Renato A, Tzioufas, Athanasios, Wieslander, J., Wiik, Anna, van der Woude, Fokko J, Hagen, Ernst Christiaan, Andrassy, Konrad, Csernok, Elena, Daha, Mohamed, Gaskin, Gill, Gross, W.L., Hansen, Bettina, Heigl, Z., Hermans, Julie, Jayne, David R.W.David, Kallenberg, Cees Gm, Lesavre, Philippe, Lockwood, Christopher Martin, Lüdemann, J., Mascart, Françoise, Mirapeix, Eduardo, Pusey, Charles Dickson, Rasmussen, Niels, Sinico, Renato A, Tzioufas, Athanasios, Wieslander, J., Wiik, Anna, and van der Woude, Fokko J

Abstract

Anti-neutrophil cytoplasmic antibodies (ANCA) are diagnostic markers for systemic vasculitis. They are classically I detected by an indirect immunofluorescence test using normal donor neutrophils as substrate. This assay lacks antigenic specificity and is not quantitative. The 'EC/BCR Project for ANCA Assay Standardization' is an international collaboration study with the aim to develop and standardize solid phase assays for ANCA detection. In this part of the study the isolation and characterization of proteinase-3 and myeloperoxidase, the two main target molecules for ANCA, and the development and standardization of ELISAs with these antigens are described. Six laboratories successfully isolated purified proteinase-3 preparations that could be used. Three of these preparations, together with one myeloperoxidase preparation, were subsequently used for ANCA testing by ELISA. The ELISA technique was standardized in two rounds of testing in the 14 participating laboratories. The coefficient of variation of these new assays decreased from values of approx. 50% in the first round to approx. 20% in the second round. We conclude that purified proteinase-3 and myeloperoxidase can be used in standardized ELISAs for ANCA detection. Whether such procedures offer advantages over the IIF test will be determined in a prospective clinical study., SCOPUS: ar.j, info:eu-repo/semantics/published

Published
1996

8. Development and standardization of solid phase assays for the detection of anti-neutrophil cytoplasmic antibodies (ANCA). A report on the second phase of an international cooperative study on the standardization of ANCA assays

Author

Hagen, Ernst Christiaan, Andrassy, Konrad, Csernok, Elena, Daha, Mohamed, Gaskin, Gill, Gross, W.L., Hansen, Bettina, Heigl, Z., Hermans, Julie, Jayne, David R.W.David, Kallenberg, Cees Gm, Lesavre, Philippe, Lockwood, Christopher Martin, Lüdemann, J., Mascart, Françoise, Mirapeix, Eduardo, Pusey, Charles Dickson, Rasmussen, Niels, Sinico, Renato A, Tzioufas, Athanasios, Wieslander, J., Wiik, Anna, van der Woude, Fokko J, Hagen, Ernst Christiaan, Andrassy, Konrad, Csernok, Elena, Daha, Mohamed, Gaskin, Gill, Gross, W.L., Hansen, Bettina, Heigl, Z., Hermans, Julie, Jayne, David R.W.David, Kallenberg, Cees Gm, Lesavre, Philippe, Lockwood, Christopher Martin, Lüdemann, J., Mascart, Françoise, Mirapeix, Eduardo, Pusey, Charles Dickson, Rasmussen, Niels, Sinico, Renato A, Tzioufas, Athanasios, Wieslander, J., Wiik, Anna, and van der Woude, Fokko J

Abstract

Anti-neutrophil cytoplasmic antibodies (ANCA) are diagnostic markers for systemic vasculitis. They are classically I detected by an indirect immunofluorescence test using normal donor neutrophils as substrate. This assay lacks antigenic specificity and is not quantitative. The 'EC/BCR Project for ANCA Assay Standardization' is an international collaboration study with the aim to develop and standardize solid phase assays for ANCA detection. In this part of the study the isolation and characterization of proteinase-3 and myeloperoxidase, the two main target molecules for ANCA, and the development and standardization of ELISAs with these antigens are described. Six laboratories successfully isolated purified proteinase-3 preparations that could be used. Three of these preparations, together with one myeloperoxidase preparation, were subsequently used for ANCA testing by ELISA. The ELISA technique was standardized in two rounds of testing in the 14 participating laboratories. The coefficient of variation of these new assays decreased from values of approx. 50% in the first round to approx. 20% in the second round. We conclude that purified proteinase-3 and myeloperoxidase can be used in standardized ELISAs for ANCA detection. Whether such procedures offer advantages over the IIF test will be determined in a prospective clinical study., SCOPUS: ar.j, info:eu-repo/semantics/published

Published
1996

9. European therapeutic trials in ANCA-associated systemic vasculitis: Disease scoring, consensus regimens and proposed clinical trials EUROPEAN COMMUNITY STUDY GROUP ON CLINICAL TRIALS IN SYSTEMIC VASCULITIS ECSYSVASTRIAL (BMHl-Cr93-1078)

Author

Rasmussen, Niels, Jayne, David R.W.David, Lockwood, Christopher Martin, Abramowicz, Daniel, Andrassy, Konrad, Bacon, Paul P.A., Savage, Caroline, Cohen Tervaert, Jan J.W., Kallenberg, Cees Gm, Dadonlené, J., Feighery, Conleth, Van Es, Leendert L.A., Hermans, Jo, van der Woude, Fokko J, Ferrario, Franco, Sinico, Renato A, Gaskin, Gill, Pusey, Charles Dickson, Gregorini, Gina, De Groot, Kirsten, Gross, Wolfgang Ludwig, Gronhagen-Riska, Carola, Guillevin, Loïc, Hagen, Ernst Christiaan, Heigl, Z., Landais, Paul, Lesavre, Philippe, Luqmani, R., Mirapeix, Eduard, Pettersson, Erna, Specks, Ulrich, Tzioufas, Athanasios, Westman, Kerstin W A, Wiik, Allan, Rasmussen, Niels, Jayne, David R.W.David, Lockwood, Christopher Martin, Abramowicz, Daniel, Andrassy, Konrad, Bacon, Paul P.A., Savage, Caroline, Cohen Tervaert, Jan J.W., Kallenberg, Cees Gm, Dadonlené, J., Feighery, Conleth, Van Es, Leendert L.A., Hermans, Jo, van der Woude, Fokko J, Ferrario, Franco, Sinico, Renato A, Gaskin, Gill, Pusey, Charles Dickson, Gregorini, Gina, De Groot, Kirsten, Gross, Wolfgang Ludwig, Gronhagen-Riska, Carola, Guillevin, Loïc, Hagen, Ernst Christiaan, Heigl, Z., Landais, Paul, Lesavre, Philippe, Luqmani, R., Mirapeix, Eduard, Pettersson, Erna, Specks, Ulrich, Tzioufas, Athanasios, Westman, Kerstin W A, and Wiik, Allan

Abstract

SCOPUS: ar.j, FLWIN, info:eu-repo/semantics/published

Published
1995

10. European therapeutic trials in ANCA-associated systemic vasculitis: Disease scoring, consensus regimens and proposed clinical trials EUROPEAN COMMUNITY STUDY GROUP ON CLINICAL TRIALS IN SYSTEMIC VASCULITIS ECSYSVASTRIAL (BMHl-Cr93-1078)

Author

Rasmussen, Niels, Jayne, David R.W.David, Lockwood, Christopher Martin, Abramowicz, Daniel, Andrassy, Konrad, Bacon, Paul P.A., Savage, Caroline, Cohen Tervaert, Jan J.W., Kallenberg, Cees Gm, Dadonlené, J., Feighery, Conleth, Van Es, Leendert L.A., Hermans, Jo, van der Woude, Fokko J, Ferrario, Franco, Sinico, Renato A, Gaskin, Gill, Pusey, Charles Dickson, Gregorini, Gina, De Groot, Kirsten, Gross, Wolfgang Ludwig, Gronhagen-Riska, Carola, Guillevin, Loïc, Hagen, Ernst Christiaan, Heigl, Z., Landais, Paul, Lesavre, Philippe, Luqmani, R., Mirapeix, Eduard, Pettersson, Erna, Specks, Ulrich, Tzioufas, Athanasios, Westman, Kerstin W A, Wiik, Allan, Rasmussen, Niels, Jayne, David R.W.David, Lockwood, Christopher Martin, Abramowicz, Daniel, Andrassy, Konrad, Bacon, Paul P.A., Savage, Caroline, Cohen Tervaert, Jan J.W., Kallenberg, Cees Gm, Dadonlené, J., Feighery, Conleth, Van Es, Leendert L.A., Hermans, Jo, van der Woude, Fokko J, Ferrario, Franco, Sinico, Renato A, Gaskin, Gill, Pusey, Charles Dickson, Gregorini, Gina, De Groot, Kirsten, Gross, Wolfgang Ludwig, Gronhagen-Riska, Carola, Guillevin, Loïc, Hagen, Ernst Christiaan, Heigl, Z., Landais, Paul, Lesavre, Philippe, Luqmani, R., Mirapeix, Eduard, Pettersson, Erna, Specks, Ulrich, Tzioufas, Athanasios, Westman, Kerstin W A, and Wiik, Allan

Abstract

SCOPUS: ar.j, FLWIN, info:eu-repo/semantics/published

Published
1995

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