Abstract
Systemic lupus erythematosus (SLE) has long been recognized to be characterized by dysregulated signaling pathways in T and B lymphocytes, beginning with observations of cellular hyperactivity and hyperresponsiveness, and evolving to recent studies focused upon the genetic and molecular bases of such phenomena. This review focuses on recently elucidated signaling abnormalities currently thought to be intrinsic to T and/or B cells in human SLE.
Publication types
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Research Support, N.I.H., Extramural
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Review
MeSH terms
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Alternative Splicing / immunology
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Animals
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Antigens, CD / immunology*
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Antigens, CD / metabolism
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B-Lymphocytes / immunology
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B-Lymphocytes / metabolism
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CD3 Complex / immunology*
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CD3 Complex / metabolism
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DNA Methylation / genetics
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DNA Methylation / immunology
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DNA-Binding Proteins / genetics*
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DNA-Binding Proteins / immunology
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DNA-Binding Proteins / metabolism
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Guanine Nucleotide Exchange Factors / genetics*
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Guanine Nucleotide Exchange Factors / immunology
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Guanine Nucleotide Exchange Factors / metabolism
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Homeostasis
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Humans
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Interleukin-2 / metabolism
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Lupus Erythematosus, Systemic / immunology*
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Lupus Erythematosus, Systemic / metabolism*
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Lymphocyte Activation / genetics
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Lymphocyte Activation / immunology*
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Membrane Microdomains / immunology
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Receptors, Antigen, T-Cell / genetics
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Receptors, Antigen, T-Cell / immunology
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Receptors, Antigen, T-Cell / metabolism*
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Signal Transduction
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T-Lymphocytes / immunology
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T-Lymphocytes / metabolism*
Substances
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Antigens, CD
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CD3 Complex
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CD3 antigen, zeta chain
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DNA-Binding Proteins
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Guanine Nucleotide Exchange Factors
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Interleukin-2
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RASGRP1 protein, human
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Receptors, Antigen, T-Cell