BCMA and Autoantibody-producing RP105 B cells ; Possible new targets of B cell therapy in systemic lupus erythematosus
Systemic lupus erythematosus (SLE) is a prototypic systemic autoimmune disease with multiple organ disorders. Although the prognosis of SLE has been recently improved, corticosteroid and immunosuppressive agents are still main treatment used in medical practice. Refractory disease and complications...
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| Published in | Japanese Journal of Clinical Immunology Vol. 35; no. 1; pp. 38 - 45 |
|---|---|
| Main Authors | , , , , , |
| Format | Journal Article |
| Language | English Japanese |
| Published |
Japan
The Japan Society for Clinical Immunology
2012
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| Subjects | |
| Online Access | Get full text |
| ISSN | 0911-4300 1349-7413 1349-7413 |
| DOI | 10.2177/jsci.35.38 |
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| Abstract | Systemic lupus erythematosus (SLE) is a prototypic systemic autoimmune disease with multiple organ disorders. Although the prognosis of SLE has been recently improved, corticosteroid and immunosuppressive agents are still main treatment used in medical practice. Refractory disease and complications by the conventional drugs still remain. RP105 (CD180) is one of the toll-like receptor associated molecules. The molecule is expressed on mature B cells. Significantly increased population of RP105-negative [RP105(−)] B cells is found in SLE. RP105(−) B cells belong to highly activated and differentiated late B cells and produce autoantibodies including anti-dsDNA antibodies. RP105(−) B cells are further divided into at least 5 subsets that include novel human B cell subsets. In active SLE, subset 1 (activated B cells) and 3 (early-plasmablasts) are significantly increased compared to inactive SLE patients. Especially, subset 3 RP105(−) B cells may play an important role in pathophysiology of SLE. RP105(−) B cells from active SLE patients express preferentially BCMA (B-cell maturation antigen) compared to BAFF-R (B-cell activating factor-receptor) than normal subjects and other autoimmune diseases. In SLE, it is suggested that BAFF/APRIL (a proliferation-inducing ligand) maintain chronic activation and survival of RP105(−) B cells. The increased RP105(−) B cells may reflect the breaking of tolerance checkpoint for autoreactive B cells and finally affect autoimmunity in SLE. For the B cell therapy, especially targeting of autoantibody-producing B cells, including subset 3 of RP105(−) B cells, BCMA and RP105(−) B cell itself may be an ideal target. |
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| AbstractList | Systemic lupus erythematosus (SLE) is a prototypic systemic autoimmune disease with multiple organ disorders. Although the prognosis of SLE has been recently improved, corticosteroid and immunosuppressive agents are still main treatment used in medical practice. Refractory disease and complications by the conventional drugs still remain. RP105 (CD180) is one of the toll-like receptor associated molecules. The molecule is expressed on mature B cells. Significantly increased population of RP105-negative [RP105(-)] B cells is found in SLE. RP105(-) B cells belong to highly activated and differentiated late B cells and produce autoantibodies including anti-dsDNA antibodies. RP105(-) B cells are further divided into at least 5 subsets that include novel human B cell subsets. In active SLE, subset 1 (activated B cells) and 3 (early-plasmablasts) are significantly increased compared to inactive SLE patients. Especially, subset 3 RP105(-) B cells may play an important role in pathophysiology of SLE. RP105(-) B cells from active SLE patients express preferentially BCMA (B-cell maturation antigen) compared to BAFF-R (B-cell activating factor-receptor) than normal subjects and other autoimmune diseases. In SLE, it is suggested that BAFF/APRIL (a proliferation-inducing ligand) maintain chronic activation and survival of RP105(-) B cells. The increased RP105(-) B cells may reflect the breaking of tolerance checkpoint for autoreactive B cells and finally affect autoimmunity in SLE. For the B cell therapy, especially targeting of autoantibody-producing B cells, including subset 3 of RP105(-) B cells, BCMA and RP105(-) B cell itself may be an ideal target. Systemic lupus erythematosus (SLE) is a prototypic systemic autoimmune disease with multiple organ disorders. Although the prognosis of SLE has been recently improved, corticosteroid and immunosuppressive agents are still main treatment used in medical practice. Refractory disease and complications by the conventional drugs still remain. RP105 (CD180) is one of the toll-like receptor associated molecules. The molecule is expressed on mature B cells. Significantly increased population of RP105-negative [RP105(-)] B cells is found in SLE. RP105(-) B cells belong to highly activated and differentiated late B cells and produce autoantibodies including anti-dsDNA antibodies. RP105(-) B cells are further divided into at least 5 subsets that include novel human B cell subsets. In active SLE, subset 1 (activated B cells) and 3 (early-plasmablasts) are significantly increased compared to inactive SLE patients. Especially, subset 3 RP105(-) B cells may play an important role in pathophysiology of SLE. RP105(-) B cells from active SLE patients express preferentially BCMA (B-cell maturation antigen) compared to BAFF-R (B-cell activating factor-receptor) than normal subjects and other autoimmune diseases. In SLE, it is suggested that BAFF/APRIL (a proliferation-inducing ligand) maintain chronic activation and survival of RP105(-) B cells. The increased RP105(-) B cells may reflect the breaking of tolerance checkpoint for autoreactive B cells and finally affect autoimmunity in SLE. For the B cell therapy, especially targeting of autoantibody-producing B cells, including subset 3 of RP105(-) B cells, BCMA and RP105(-) B cell itself may be an ideal target.Systemic lupus erythematosus (SLE) is a prototypic systemic autoimmune disease with multiple organ disorders. Although the prognosis of SLE has been recently improved, corticosteroid and immunosuppressive agents are still main treatment used in medical practice. Refractory disease and complications by the conventional drugs still remain. RP105 (CD180) is one of the toll-like receptor associated molecules. The molecule is expressed on mature B cells. Significantly increased population of RP105-negative [RP105(-)] B cells is found in SLE. RP105(-) B cells belong to highly activated and differentiated late B cells and produce autoantibodies including anti-dsDNA antibodies. RP105(-) B cells are further divided into at least 5 subsets that include novel human B cell subsets. In active SLE, subset 1 (activated B cells) and 3 (early-plasmablasts) are significantly increased compared to inactive SLE patients. Especially, subset 3 RP105(-) B cells may play an important role in pathophysiology of SLE. RP105(-) B cells from active SLE patients express preferentially BCMA (B-cell maturation antigen) compared to BAFF-R (B-cell activating factor-receptor) than normal subjects and other autoimmune diseases. In SLE, it is suggested that BAFF/APRIL (a proliferation-inducing ligand) maintain chronic activation and survival of RP105(-) B cells. The increased RP105(-) B cells may reflect the breaking of tolerance checkpoint for autoreactive B cells and finally affect autoimmunity in SLE. For the B cell therapy, especially targeting of autoantibody-producing B cells, including subset 3 of RP105(-) B cells, BCMA and RP105(-) B cell itself may be an ideal target. Systemic lupus erythematosus (SLE) is a prototypic systemic autoimmune disease with multiple organ disorders. Although the prognosis of SLE has been recently improved, corticosteroid and immunosuppressive agents are still main treatment used in medical practice. Refractory disease and complications by the conventional drugs still remain. RP105 (CD180) is one of the toll-like receptor associated molecules. The molecule is expressed on mature B cells. Significantly increased population of RP105-negative [RP105(−)] B cells is found in SLE. RP105(−) B cells belong to highly activated and differentiated late B cells and produce autoantibodies including anti-dsDNA antibodies. RP105(−) B cells are further divided into at least 5 subsets that include novel human B cell subsets. In active SLE, subset 1 (activated B cells) and 3 (early-plasmablasts) are significantly increased compared to inactive SLE patients. Especially, subset 3 RP105(−) B cells may play an important role in pathophysiology of SLE. RP105(−) B cells from active SLE patients express preferentially BCMA (B-cell maturation antigen) compared to BAFF-R (B-cell activating factor-receptor) than normal subjects and other autoimmune diseases. In SLE, it is suggested that BAFF/APRIL (a proliferation-inducing ligand) maintain chronic activation and survival of RP105(−) B cells. The increased RP105(−) B cells may reflect the breaking of tolerance checkpoint for autoreactive B cells and finally affect autoimmunity in SLE. For the B cell therapy, especially targeting of autoantibody-producing B cells, including subset 3 of RP105(−) B cells, BCMA and RP105(−) B cell itself may be an ideal target. |
| Author | KOARADA, Syuichi SUEMATSU, Rie TASHIRO, Satoko INOUE, Hisako OHTA, Akihide TADA, Yoshifumi |
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| Cites_doi | 10.1517/14656560902946419 10.1002/1529-0131(199912)42:12<2593::AID-ANR12>3.0.CO;2-G 10.1093/rheumatology/40.11.1315 10.1093/rheumatology/kep437 10.1016/j.chom.2008.12.002 10.1002/art.10672 10.2165/00128072-200204040-00004 10.1016/S0140-6736(10)61354-2 10.1084/jem.180.4.1217 10.1084/jem.20031330 10.1136/ard.60.12.1137 10.1002/art.23047 |
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| References | 3) Blumenthal A, Kobayashi T, Pierini LM, Banaei N, Ernst JD, Miyake K, Ehrt S. : RP105 facilitates macrophage activation by Mycobacterium tuberculosis lipoproteins. Cell Host Microbe. 5 : 35-46, 2009. 14) Grammer AC, Lipsky PE. : B cell abnormalities in systemic lupus erythematosus. Arthritis Res Ther. 5 (Suppl 4) : S22-27, 2003. 8) O'Connor BP, Raman VS, Erickson LD, Cook WJ, Weaver LK, Ahonen C, Lin LL, Mantchev GT, Bram RJ, Noelle RJ. : J BCMA is essential for the survival of long-lived bone marrow plasma cells. Exp Med. 199 : 91-98, 2004. 13) Koarada S, Tada Y, Suematsu R, Soejima S, Inoue H, Ohta A, Nagasawa K. : Phenotyping of P105-negative B cell subsets in patients with systemic lupus erythematosus. Clin Dev Immunol. 2012 : 198206, 2012. [Epub 2011 Sep 26]. 11) Carreño L, López-Longo FJ, González CM, Monteagudo I. : Treatment options for juvenile-onset systemic lupus erythematosus. Paediatr Drugs. 4 : 241-256, 2002. 19) Koarada S, Tada Y, Kikuchi Y, Ushiyama O, Suzuki N, Ohta A, Nagasawa K. : CD180 (RP105) in rheumatic diseases. Rheumatology (Oxford). 40 : 1315-1316, 2001. 12) Horowitz DM, Furie RA. : Abetimus sodium : a medication for the prevention of lupus nephritis flares. Expert Opin Pharmacother. 10 : 1501-1507, 2009. 17) Kikuchi Y, Koarada S, Tada Y, Ushiyama O, Morito F, Suzuki N, Ohta A, Horiuchi T, Miyake K, Nagasawa K. : Difference in B cell activation between dermatomyositis and polymyositis : analysis of the expression of RP105 on peripheral blood B cells. Ann Rheum Dis. 60 : 1137-1140, 2001. 1) Miyake K, Yamashita Y, Ogata M, Sudo T, Kimoto M. : RP105, a novel B cell surface molecule implicated in B cell activation, is a member of the leucine-rich repeat protein family. J Immunol. 154 : 3333-3340, 1995. 2) Miyake K, Yamashita Y, Hitoshi Y, et al. : Murine B cell proliferation and protection from apoptosis with an antibody against a 105-kD molecule : unresponsiveness of X-linked immunodeficient B cells. J Exp Med 180 : 1217-1224, 1994. 7) Kikuchi Y, Koarada S, Tada Y, Ushiyama O, Morito F, Suzuki N, Ohta A, Miyake K, Kimoto M, Horiuchi T, Nagasawa K. : RP105-lacking B cells from lupus patients are responsible for the production of immunoglobulins and autoantibodies. Arthritis Rheum. 46 : 3259-3265, 2002. 9) Koarada S. : Autoantibody-producing B cells and B cell therapy in systemic lupus erythematosus. -Possible new targets of novel subsets of RP105-negative B cells- in Lupus : Symptoms, Treatment and Potential Complications. Novascience publishers. 2012 (in press 6) Koarada S, Ide M, Haruta Y, Tada Y, Ushiyama O, Morito F, Ohta A, Nagasawa K. : Two cases of antinuclear antibody negative lupus showing increased proportion of B cells lacking RP105. J Rheumatol. 32 : 562-564, 2005. 16) Dall'Era M, Chakravarty E, Wallace D, Genovese M, Weisman M, Kavanaugh A, Kalunian K, Dhar P, Vincent E, Pena-Rossi C, Wofsy D. : Reduced B lymphocyte and immunoglobulin levels after atacicept treatment in patients with systemic lupus erythematosus : results of a multicenter, phase Ib, double-blind, placebo-controlled, dose-escalating trial. Arthritis Rheum. 56 : 4142-4150, 2007. 20) Koarada S, Tada Y. : RP105-negative B cells in systemic lupus erythematosus. Clin Dev Immunol. 2012 : 259186, 2012. [Epub 2011 Sep 15]. 10) Koarada S, Tada Y, Sohma Y, Haruta Y, Suematsu R, Mitamura M, Inoue H, Ehara H, Tokoro Y, Ohta A, Nagasawa K. : Autoantibody-producing RP105(−) B cells, from patients with systemic lupus erythematosus, showed more preferential expression of BCMA compared with BAFF-R than normal subjects. Rheumatology (Oxford). 49 : 662-670, 2010. 4) Tada Y, Koarada S, Morito F, Mitamura M, Inoue H, Suematsu R, Ohta A, Miyake K, Nagasawa K. : Toll-like receptor homolog RP105 modulates the antigen-presenting cell function and regulates the development of collagen-induced arthritis. Arthritis Res Ther. 10 : R121, 2008. [Epub 2008 Oct 11] 15) Navarra SV, Guzmán RM, Gallacher AE, Hall S, Levy RA, Jimenez RE, Li EK, Thomas M, Kim HY, León MG, Tanasescu C, Nasonov E, Lan JL, Pineda L, Zhong ZJ, Freimuth W, Petri MA. : BLISS-52 Study Group. Efficacy and safety of belimumab in patients with active systemic lupus erythematosus : a randomised, placebo-controlled, phase 3 trial. Lancet. 377 : 721-731, 2011. 5) Koarada S, Tada Y, Ushiyama O, Morito F, Suzuki N, Ohta A, Miyake K, Kimoto M, Nagasawa K. : B cells lacking RP105, a novel B cell antigen, in systemic lupus erythematosus. Arthritis Rheum. 42 : 2593-2600, 1999. 18) Kikuchi Y, Koarada S, Nakamura S, Yonemitsu N, Tada Y, Haruta Y, Morito F, Ohta A, Miyake K, Horiuchi T, Nagasawa K. : Increase of RP105-lacking activated B cells in the peripheral blood and salivary glands in patients with Sjögren's syndrome. Clin Exp Rheumatol. 26 : 5-12, 2008. Carreño L, Ló (11) 2002; 4 14 Koarada S, Tada Y, Ushiyama O, Mori (5) 1999; 42 15 Horowitz DM, Furie RA. (12) 2009; 10 17 Koarada S, Tada Y. (20) 2012; 2012 Koarada S, Tada Y, Kikuchi Y, Ushiy (19) 2001; 40 Koarada S, Tada Y, Suematsu R, Soej (13) 2012; 2012 1 2 Kikuchi Y, Koarada S, Tada Y, Ushiy (7) 2002; 46 4 Dall'Era M, Chakravarty E, Wal (16) 2007; 56 Kikuchi Y, Koarada S, Nakamura S, Y (18) 2008; 26 9 Koarada S, Ide M, Haruta Y, Tada Y (6) 2005; 32 Blumenthal A, Kobayashi T, Pierini (3) 2009; 5 O'Connor BP, Raman VS, Erickso (8) 2004; 199 10 |
| References_xml | – reference: 1) Miyake K, Yamashita Y, Ogata M, Sudo T, Kimoto M. : RP105, a novel B cell surface molecule implicated in B cell activation, is a member of the leucine-rich repeat protein family. J Immunol. 154 : 3333-3340, 1995. – reference: 19) Koarada S, Tada Y, Kikuchi Y, Ushiyama O, Suzuki N, Ohta A, Nagasawa K. : CD180 (RP105) in rheumatic diseases. Rheumatology (Oxford). 40 : 1315-1316, 2001. – reference: 14) Grammer AC, Lipsky PE. : B cell abnormalities in systemic lupus erythematosus. Arthritis Res Ther. 5 (Suppl 4) : S22-27, 2003. – reference: 18) Kikuchi Y, Koarada S, Nakamura S, Yonemitsu N, Tada Y, Haruta Y, Morito F, Ohta A, Miyake K, Horiuchi T, Nagasawa K. : Increase of RP105-lacking activated B cells in the peripheral blood and salivary glands in patients with Sjögren's syndrome. Clin Exp Rheumatol. 26 : 5-12, 2008. – reference: 20) Koarada S, Tada Y. : RP105-negative B cells in systemic lupus erythematosus. Clin Dev Immunol. 2012 : 259186, 2012. [Epub 2011 Sep 15]. – reference: 9) Koarada S. : Autoantibody-producing B cells and B cell therapy in systemic lupus erythematosus. -Possible new targets of novel subsets of RP105-negative B cells- in Lupus : Symptoms, Treatment and Potential Complications. Novascience publishers. 2012 (in press) – reference: 7) Kikuchi Y, Koarada S, Tada Y, Ushiyama O, Morito F, Suzuki N, Ohta A, Miyake K, Kimoto M, Horiuchi T, Nagasawa K. : RP105-lacking B cells from lupus patients are responsible for the production of immunoglobulins and autoantibodies. Arthritis Rheum. 46 : 3259-3265, 2002. – reference: 17) Kikuchi Y, Koarada S, Tada Y, Ushiyama O, Morito F, Suzuki N, Ohta A, Horiuchi T, Miyake K, Nagasawa K. : Difference in B cell activation between dermatomyositis and polymyositis : analysis of the expression of RP105 on peripheral blood B cells. Ann Rheum Dis. 60 : 1137-1140, 2001. – reference: 2) Miyake K, Yamashita Y, Hitoshi Y, et al. : Murine B cell proliferation and protection from apoptosis with an antibody against a 105-kD molecule : unresponsiveness of X-linked immunodeficient B cells. J Exp Med 180 : 1217-1224, 1994. – reference: 3) Blumenthal A, Kobayashi T, Pierini LM, Banaei N, Ernst JD, Miyake K, Ehrt S. : RP105 facilitates macrophage activation by Mycobacterium tuberculosis lipoproteins. Cell Host Microbe. 5 : 35-46, 2009. – reference: 11) Carreño L, López-Longo FJ, González CM, Monteagudo I. : Treatment options for juvenile-onset systemic lupus erythematosus. Paediatr Drugs. 4 : 241-256, 2002. – reference: 15) Navarra SV, Guzmán RM, Gallacher AE, Hall S, Levy RA, Jimenez RE, Li EK, Thomas M, Kim HY, León MG, Tanasescu C, Nasonov E, Lan JL, Pineda L, Zhong ZJ, Freimuth W, Petri MA. : BLISS-52 Study Group. Efficacy and safety of belimumab in patients with active systemic lupus erythematosus : a randomised, placebo-controlled, phase 3 trial. Lancet. 377 : 721-731, 2011. – reference: 4) Tada Y, Koarada S, Morito F, Mitamura M, Inoue H, Suematsu R, Ohta A, Miyake K, Nagasawa K. : Toll-like receptor homolog RP105 modulates the antigen-presenting cell function and regulates the development of collagen-induced arthritis. Arthritis Res Ther. 10 : R121, 2008. [Epub 2008 Oct 11] – reference: 6) Koarada S, Ide M, Haruta Y, Tada Y, Ushiyama O, Morito F, Ohta A, Nagasawa K. : Two cases of antinuclear antibody negative lupus showing increased proportion of B cells lacking RP105. J Rheumatol. 32 : 562-564, 2005. – reference: 8) O'Connor BP, Raman VS, Erickson LD, Cook WJ, Weaver LK, Ahonen C, Lin LL, Mantchev GT, Bram RJ, Noelle RJ. : J BCMA is essential for the survival of long-lived bone marrow plasma cells. Exp Med. 199 : 91-98, 2004. – reference: 12) Horowitz DM, Furie RA. : Abetimus sodium : a medication for the prevention of lupus nephritis flares. Expert Opin Pharmacother. 10 : 1501-1507, 2009. – reference: 13) Koarada S, Tada Y, Suematsu R, Soejima S, Inoue H, Ohta A, Nagasawa K. : Phenotyping of P105-negative B cell subsets in patients with systemic lupus erythematosus. Clin Dev Immunol. 2012 : 198206, 2012. [Epub 2011 Sep 26]. – reference: 5) Koarada S, Tada Y, Ushiyama O, Morito F, Suzuki N, Ohta A, Miyake K, Kimoto M, Nagasawa K. : B cells lacking RP105, a novel B cell antigen, in systemic lupus erythematosus. Arthritis Rheum. 42 : 2593-2600, 1999. – reference: 10) Koarada S, Tada Y, Sohma Y, Haruta Y, Suematsu R, Mitamura M, Inoue H, Ehara H, Tokoro Y, Ohta A, Nagasawa K. : Autoantibody-producing RP105(−) B cells, from patients with systemic lupus erythematosus, showed more preferential expression of BCMA compared with BAFF-R than normal subjects. Rheumatology (Oxford). 49 : 662-670, 2010. – reference: 16) Dall'Era M, Chakravarty E, Wallace D, Genovese M, Weisman M, Kavanaugh A, Kalunian K, Dhar P, Vincent E, Pena-Rossi C, Wofsy D. : Reduced B lymphocyte and immunoglobulin levels after atacicept treatment in patients with systemic lupus erythematosus : results of a multicenter, phase Ib, double-blind, placebo-controlled, dose-escalating trial. Arthritis Rheum. 56 : 4142-4150, 2007. – ident: 4 – volume: 10 start-page: 1501 issn: 1465-6566 year: 2009 ident: 12 publication-title: Expert Opin Pharmacother doi: 10.1517/14656560902946419 – ident: 1 – volume: 42 start-page: 2593 issn: 0004-3591 year: 1999 ident: 5 publication-title: Arthritis Rheum doi: 10.1002/1529-0131(199912)42:12<2593::AID-ANR12>3.0.CO;2-G – volume: 40 start-page: 1315 issn: 1462-0324 year: 2001 ident: 19 publication-title: Rheumatology (Oxford) doi: 10.1093/rheumatology/40.11.1315 – ident: 10 doi: 10.1093/rheumatology/kep437 – volume: 26 start-page: 5 issn: 0392-856X year: 2008 ident: 18 publication-title: Clin Exp Rheumatol – volume: 5 start-page: 35 issn: 1931-3128 year: 2009 ident: 3 publication-title: Cell Host Microbe doi: 10.1016/j.chom.2008.12.002 – volume: 46 start-page: 3259 issn: 0004-3591 year: 2002 ident: 7 publication-title: Arthritis Rheum doi: 10.1002/art.10672 – volume: 4 start-page: 241 issn: 1174-5878 year: 2002 ident: 11 publication-title: Paediatr Drugs doi: 10.2165/00128072-200204040-00004 – ident: 15 doi: 10.1016/S0140-6736(10)61354-2 – ident: 14 – ident: 2 doi: 10.1084/jem.180.4.1217 – volume: 32 start-page: 562 issn: 0315-162X year: 2005 ident: 6 publication-title: J Rheumatol – volume: 2012 start-page: 259186 issn: 1740-2522 year: 2012 ident: 20 publication-title: Clin Dev Immunol. – volume: 199 start-page: 91 issn: 0040-8727 year: 2004 ident: 8 publication-title: Exp Med doi: 10.1084/jem.20031330 – ident: 9 – volume: 2012 start-page: 198206 issn: 1740-2522 year: 2012 ident: 13 publication-title: Clin Dev Immunol. – ident: 17 doi: 10.1136/ard.60.12.1137 – volume: 56 start-page: 4142 issn: 0004-3591 year: 2007 ident: 16 publication-title: Arthritis Rheum doi: 10.1002/art.23047 |
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| SubjectTerms | Antibody Formation Autoantibodies - biosynthesis Autoantibodies - immunology B cell B-Cell Maturation Antigen - immunology B-Lymphocytes - immunology BCMA Cell- and Tissue-Based Therapy Humans Lupus Erythematosus, Systemic - immunology Lupus Erythematosus, Systemic - therapy plasmablast RP105 SLE |
| Title | BCMA and Autoantibody-producing RP105 B cells ; Possible new targets of B cell therapy in systemic lupus erythematosus |
| URI | https://www.jstage.jst.go.jp/article/jsci/35/1/35_1_38/_article/-char/en https://www.ncbi.nlm.nih.gov/pubmed/22374441 https://www.proquest.com/docview/925717006 |
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| ispartofPNX | Japanese Journal of Clinical Immunology, 2012, Vol.35(1), pp.38-45 |
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