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Article: The immunological basis of B-cell therapy in systemic lupus erythematosus

TitleThe immunological basis of B-cell therapy in systemic lupus erythematosus
Authors
KeywordsB lymphocytes
Biologic treatment
Pathogenesis
Systemic lupus erythematosus
Issue Date2010
PublisherWiley-Blackwell Publishing Asia. The Journal's web site is located at http://www.blackwell-synergy.com/loi/ijrd
Citation
International Journal Of Rheumatic Diseases, 2010, v. 13 n. 1, p. 3-11 How to Cite?
AbstractLoss of B-cell tolerance is a hallmark feature of the pathogenesis in systemic lupus erythematosus (SLE), an autoimmune disease that is characterized by hypergammaglobulinemia and autoantibody production. These autoantibodies lead to formation of immune-complex deposition in internal organs causing inflammation and damage. Autoreactive B-cells are believed to be central in the pathophysiology of SLE. Other than its role in the production of antibodies that mediate humoral immune response, B-cells also function as antigen-presenting cells and are capable of activating T-cells. Activated B-cells may also produce pro-inflammatory cytokines that aggravate local inflammation. Abnormal B-cell homeostasis has been described in SLE patients. This may occur as a result of intrinsic B-cell defect or from aberrant regulation by maturation and survival signals. B-cell-based therapy is the current mainstream of research and development of novel therapies in SLE patients with severe and refractory disease. Potential cellular and molecular targets for B-cell therapies include cell surface molecules such as CD20 (rituximab) and CD22 (epratuzumab); co-stimulatory molecules involved in B-cell-T-cell interaction such as CTLA4 and B7 molecules (abatacept); maturation and growth factors such as B-cell activating factor and a proliferation-inducing ligand (belimumab, briobacept, atacicept) and B-cell tolerogen (abetimus). This article provides an overview on normal B-cell physiology and abnormal B-cell biology in SLE that form the immunological basis of B-cell-targeted therapy in the treatment of these patients with refractory diseases. © Asia Pacific League of Associations for Rheumatology.
Persistent Identifierhttp://hdl.handle.net/10722/124960
ISSN
2015 Impact Factor: 1.914
2015 SCImago Journal Rankings: 0.536
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorMok, MYen_HK
dc.date.accessioned2010-10-31T11:03:43Z-
dc.date.available2010-10-31T11:03:43Z-
dc.date.issued2010en_HK
dc.identifier.citationInternational Journal Of Rheumatic Diseases, 2010, v. 13 n. 1, p. 3-11en_HK
dc.identifier.issn1756-1841en_HK
dc.identifier.urihttp://hdl.handle.net/10722/124960-
dc.description.abstractLoss of B-cell tolerance is a hallmark feature of the pathogenesis in systemic lupus erythematosus (SLE), an autoimmune disease that is characterized by hypergammaglobulinemia and autoantibody production. These autoantibodies lead to formation of immune-complex deposition in internal organs causing inflammation and damage. Autoreactive B-cells are believed to be central in the pathophysiology of SLE. Other than its role in the production of antibodies that mediate humoral immune response, B-cells also function as antigen-presenting cells and are capable of activating T-cells. Activated B-cells may also produce pro-inflammatory cytokines that aggravate local inflammation. Abnormal B-cell homeostasis has been described in SLE patients. This may occur as a result of intrinsic B-cell defect or from aberrant regulation by maturation and survival signals. B-cell-based therapy is the current mainstream of research and development of novel therapies in SLE patients with severe and refractory disease. Potential cellular and molecular targets for B-cell therapies include cell surface molecules such as CD20 (rituximab) and CD22 (epratuzumab); co-stimulatory molecules involved in B-cell-T-cell interaction such as CTLA4 and B7 molecules (abatacept); maturation and growth factors such as B-cell activating factor and a proliferation-inducing ligand (belimumab, briobacept, atacicept) and B-cell tolerogen (abetimus). This article provides an overview on normal B-cell physiology and abnormal B-cell biology in SLE that form the immunological basis of B-cell-targeted therapy in the treatment of these patients with refractory diseases. © Asia Pacific League of Associations for Rheumatology.en_HK
dc.languageengen_HK
dc.publisherWiley-Blackwell Publishing Asia. The Journal's web site is located at http://www.blackwell-synergy.com/loi/ijrden_HK
dc.relation.ispartofInternational Journal of Rheumatic Diseasesen_HK
dc.rightsThe definitive version is available at www3.interscience.wiley.com-
dc.subjectB lymphocytesen_HK
dc.subjectBiologic treatmenten_HK
dc.subjectPathogenesisen_HK
dc.subjectSystemic lupus erythematosusen_HK
dc.subject.meshAutoimmunity-
dc.subject.meshB-Lymphocytes - immunology-
dc.subject.meshImmune Tolerance-
dc.subject.meshImmunotherapy - methods-
dc.subject.meshLupus Erythematosus, Systemic - immunology - therapy-
dc.titleThe immunological basis of B-cell therapy in systemic lupus erythematosusen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1756-1841&volume=13&issue=1&spage=3&epage=11&date=2010&atitle=The+immunological+basis+of+B+cell+therapy+in+systemic+lupus+erythematosus-
dc.identifier.emailMok, MY:temy@hkucc.hku.hken_HK
dc.identifier.authorityMok, MY=rp00490en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1111/j.1756-185X.2009.01458.xen_HK
dc.identifier.pmid20374380-
dc.identifier.scopuseid_2-s2.0-75649121143en_HK
dc.identifier.hkuros174109en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-75649121143&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume13en_HK
dc.identifier.issue1en_HK
dc.identifier.spage3en_HK
dc.identifier.epage11en_HK
dc.identifier.isiWOS:000274147400002-
dc.publisher.placeAustraliaen_HK
dc.identifier.scopusauthoridMok, MY=7006024184en_HK

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