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Lupus pp 140–151Cite as

Murine Graft-vs-Host Disease

Relevance to Human Lupus Immunopathogenesis and Therapy

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Part of the book series: Contemporary Immunology ((CONTIM))

Abstract

Systemic lupus erythematosus (SLE) is a disease characterized by B-cell hyperactivity leading to auto-antibody production and deposition in target organs. Pathogenic autoantibodies are typically of the IgG class, a T-cell—dependent isotype, suggesting that the polyclonal B-cell hyperactivity in SLE is T-cell—driven. Studies of T-cell function in humans with SLE have reported a number of diverse and occasionally contradictory immunologic defects (reviewed in ref. 1). It must be kept in mind that studies using human SLE patients are complicated by several factors:

  1. 1.

    There is variability in disease expression among patients; e.g., patients with predominantly renal disease may have different immunopathogenic mechanisms than patients with primarily central nervous system involvement.

  2. 2.

    It is difficult to stage disease activity accurately, hindering reliable comparisons between patients.

  3. 3.

    The effect of medications, many of which are immunosuppressive, must be taken into account.

  4. 4.

    In most instances, studies have been done using patients with active disease; thus, it is not known whether a given defect in immune function is responsible for the initiation of SLE or is instead a consequence of the disease or its treatment.

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Shustov, A., Rus, V., Nguyen, P., Via, C.S. (1999). Murine Graft-vs-Host Disease. In: Kammer, G.M., Tsokos, G.C. (eds) Lupus. Contemporary Immunology. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-59259-703-1_9

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  • DOI: https://doi.org/10.1007/978-1-59259-703-1_9

  • Publisher Name: Humana Press, Totowa, NJ

  • Print ISBN: 978-1-4757-5686-9

  • Online ISBN: 978-1-59259-703-1

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