NDLI: Chronic exposure to staphylococcal superantigen elicits a systemic inflammatory disease mimicking lupus.

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Chronic exposure to staphylococcal superantigen elicits a systemic inflammatory disease mimicking lupus.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Rajagopalan, Govindarajan Tilahun, Ashenafi Y. Clark, Chad R. Chowdhary, Vaidehi R. Grande, Joseph P.
Description	Country affiliation: United States Author Affiliation: Chowdhary VR ( Division of Rheumatology, Department of Medicine, Mayo Clinic, Rochester, MN 55905, USA. chowdhary.vaidehi@mayo.edu)
Abstract	Chronic nasal and skin colonization with superantigen (SAg)-producing Staphylococcus aureus is well documented in humans. Given that trans-mucosal and trans-cutaneous absorption of SAgs can occur, we determined whether chronic exposure to small amounts of SAg per se could activate autoreactive CD4(+) and CD8(+) T cells and precipitate any autoimmune disease without further external autoantigenic stimulation. Because HLA class II molecules present SAg more efficiently than do mouse MHC class II molecules, HLA-DQ8 transgenic mice were implanted s.c. with mini-osmotic pumps capable of continuously delivering the SAg, staphylococcal enterotoxin B (total of 10 µg/mouse), or PBS over 4 wk. Chronic exposure to staphylococcal enterotoxin B resulted in a multisystem autoimmune inflammatory disease with features similar to systemic lupus erythematosus. The disease was characterized by mononuclear cell infiltration of lungs, liver, and kidneys, accompanied by the production of anti-nuclear Abs and deposition of immune complexes in the renal glomeruli. The inflammatory infiltrates in various organs predominantly consisted of CD4(+) T cells bearing TCR Vß8. The extent of immunopathology was markedly reduced in mice lacking CD4(+) T cells and CD28, indicating that the disease is CD4(+) T cell mediated and CD28 dependent. The absence of disease in STAT4-deficient, as well as IFN-Î³-deficient, HLA-DQ8 mice suggested the pathogenic role of Th1-type cytokines, IL-12 and IFN-Î³. In conclusion, our study suggests that chronic exposure to extremely small amounts of bacterial SAg could be an etiological factor for systemic lupus erythematosus.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1201097
Journal	The Journal of Immunology
Issue Number	4
Volume Number	189
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2012-08-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Autoimmune Diseases Immunology Cd4-positive T-lymphocytes Lupus Erythematosus, Systemic Superantigens Animals Antigens, Cd28 Autoantibodies Blood Autoantigens Pathology Enzyme-linked Immunosorbent Assay Flow Cytometry Fluorescent Antibody Technique Hla-dq Antigens Infusions, Subcutaneous Mice Mice, Transgenic Staphylococcus Aureus Administration & Dosage Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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Chronic exposure to staphylococcal superantigen elicits a systemic inflammatory disease mimicking lupus.