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Macrophage i-a/i-e expression and macrophage-stimulating lymphokines in murine lupus

Academic Article
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Overview

authors

  • Kofler, R.
  • Schreiber, R. D.
  • Dixon, F. J.
  • Theofilopoulos, Argyrios

publication date

  • 1984

journal

  • Cellular Immunology  Journal

abstract

  • Seeking common abnormalities in mice genetically predisposed to lupus-like autoimmune disease, we investigated (1) the ontogeny of Ia antigens (I-A/I-E) on the surfaces of resident peritoneal macrophages (rpM phi) of lupus and normal mice, (2) spontaneous and lectin-induced in vitro production of M phi-stimulating factors (interferon, IFN; M phi-activating factor, MAF; M phi-Ia-inducing/recruiting factor, MIRF), and (3) responses of rpM phi from such animals to Ia-inducing signals. Indirect immunofluorescence techniques showed that Ia+ rpM phi increased numerically during the life spans of MRL/Mp lpr/lpr, while no such increase was observed in age-matched non-lpr MRL/Mp +/+ or (MRL/Mp lpr/lpr X MRL/Mp +/+)F1 hybrid mice. However, neonatal thymectomy, which prevents lymphoproliferation and autoimmune disease in MRL/Mp lpr/lpr mice, had no effect on this enhanced M phi I-A/I-E expression. NZB mice developed a similar increase with age, whereas BXSB and (NZB X NZW)F1 lupus mice, like immunologically normal controls, had low numbers of I-A/I-E+ rpM phi. Cultured splenocytes of lupus mice, including those with high percentages of I-A/I-E+ rpM phi, did not spontaneously (in the absence of mitogens) elaborate MIRF, MAF, or IFN activity. Furthermore, concanavalin A-stimulated splenocytes from lupus mice, particularly strains with early autoimmune disease manifestations [MRL/Mp lpr/lpr, male BXSB, and female (NZB X NZW)F1] produced levels of these lymphokines that were lower than normal controls. MRL/Mp lpr/lpr and NZB rpM phi, when stimulated in vitro with the supernatant of a MIRF-producing T cell hybridoma, did not hyperrespond. Our study shows that increased I-A/I-E+ rpM phi occur in some, but not all, lupus mice and this increase does not correlate with increased spontaneous or mitogen-induced production of M phi-stimulating lymphokines nor with hyperresponsiveness to Ia-inducing signals.

subject areas

  • Aging
  • Animals
  • Female
  • Genes, MHC Class II
  • Histocompatibility Antigens Class II
  • Interferons
  • Lupus Erythematosus, Systemic
  • Lymphocyte Activation
  • Lymphokines
  • Macrophage Activation
  • Macrophage-Activating Factors
  • Macrophages
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Mice, Inbred C3H
  • Mice, Inbred C57BL
  • Mice, Inbred DBA
  • Mice, Inbred NZB
  • Mice, Mutant Strains
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Identity

International Standard Serial Number (ISSN)

  • 0008-8749

Digital Object Identifier (DOI)

  • 10.1016/0008-8749(84)90133-3

PubMed ID

  • 6204780
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Additional Document Info

start page

  • 92

end page

  • 100

volume

  • 87

issue

  • 1

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