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[PMID]: | 28644972 |
[Au] Autor: | Adem J; Eray M; Eeva J; Nuutinen U; Pelkonen J |
[Ad] Endereço: | Department of Clinical Microbiology, Institute of Clinical Medicine, University of Eastern Finland, Yliopistonranta 1C, 70210 Kuopio, Finland. Electronic address: jemal.adem@uef.fi. |
[Ti] Título: | Advantages of targeting B cell receptor complex to treat B-cell derived autoimmune diseases and lymphomas. |
[So] Source: | Mol Immunol;88:135-137, 2017 Aug. | [Is] ISSN: | 1872-9142 |
[Cp] País de publicação: | England |
[La] Idioma: | eng |
[Ab] Resumo: | Antibodies produced by B-cells provide protection from infectious agents. However, impaired cell death signaling pathways in B-cells can lead to cancer, immunodeficiency or autoimmune diseases. B-cell signaling molecules such as CD20, CD19, Btk, and BAFF-R are targeted by therapeutic drugs and used to treat B-cell derived lymphomas or autoimmune diseases. Nevertheless, B-cells could develop resistance to these therapeutic drugs or the therapeutic drugs may have off-target effects. For instance, repeated rituximab (anti-CD20 antibody) treatment may lead to the loss of its target cell surface molecule, CD20. In addition, in B-cell malignancies, loss of CD19 expression has been observed. Another target molecule, Btk is expressed not only in B-cells but also in mast cells, macrophages, and dendritic cells. Thus, targeting Btk could negatively regulate the functions of innate immunity. The expression of BAFF-R is thought to be restricted to B-cells but it is also expressed on T-cells. Targeting BAFF-R, therefore, may lead to depletion of T-cells in addition to B-cells. B cell receptor (BCR) expression and signaling, however, are critically important for development, differentiation and survival of B-cells. Moreover, BCR is exclusively expressed on B-cells, which makes it an excellent target to avoid off-target effects. |
[Mh] Termos MeSH primário: |
Antígenos CD19/metabolismo Antígenos CD20/metabolismo Doenças Autoimunes/tratamento farmacológico Linfócitos B/imunologia Linfoma de Células B/tratamento farmacológico Proteínas Proto-Oncogênicas c-bcr/metabolismo Rituximab/uso terapêutico
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[Mh] Termos MeSH secundário: |
Doenças Autoimunes/patologia Receptor do Fator Ativador de Células B/metabolismo Resistência a Medicamentos Antineoplásicos Seres Humanos Linfoma de Células B/patologia Proteínas Tirosina Quinases/metabolismo
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[Pt] Tipo de publicação: | LETTER |
[Nm] Nome de substância:
| 0 (Antigens, CD19); 0 (Antigens, CD20); 0 (B-Cell Activation Factor Receptor); 0 (TNFRSF13C protein, human); 4F4X42SYQ6 (Rituximab); EC 2.7.10.1 (Agammaglobulinaemia tyrosine kinase); EC 2.7.10.1 (Protein-Tyrosine Kinases); EC 2.7.11.1 (BCR protein, human); EC 2.7.11.1 (Proto-Oncogene Proteins c-bcr) |
[Em] Mês de entrada: | 1710 |
[Cu] Atualização por classe: | 171009 |
[Lr] Data última revisão:
| 171009 |
[Sb] Subgrupo de revista: | IM |
[Da] Data de entrada para processamento: | 170624 |
[St] Status: | MEDLINE |
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