The natural killer cell - Friend or foe in autoimmune disease?

M. Flodström, F. D. Shi, Nora E Sarvetnick, H. G. Ljunggren

Research output: Contribution to journalReview article

72 Citations (Scopus)

Abstract

Autoimmune diseases are chronic conditions resulting from a loss of immunological tolerance to self-antigens. Recent observations have supported an ever-broader role for innate immune responses in directing and regulating adaptive immunity, including responses to self. This review summarizes recent findings supporting important functions of natural killer (NK) cells in regulating autoimmunity. A close survey of the current literature reveals multiple steps where NK cells can regulate inflammation and intervene in loss of self-tolerance. Importantly, the findings also caution against inferring a similar role for NK cells in all autoimmune phenomena or during separate stages of the same disease. Indeed, NK cells may have different influences during the priming and the effector phases of disease. Hence, an increased understanding of the involvement of NK cells in inflammation and infection should provide new insights into the pathogenesis of autoimmune disease.

Original languageEnglish (US)
Pages (from-to)432-441
Number of pages10
JournalScandinavian Journal of Immunology
Volume55
Issue number5
DOIs
StatePublished - May 8 2002
Externally publishedYes

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Natural Killer Cells
Autoimmune Diseases
Inflammation
Self Tolerance
Autoantigens
Adaptive Immunity
Autoimmunity
Innate Immunity
Infection

ASJC Scopus subject areas

  • Immunology

Cite this

The natural killer cell - Friend or foe in autoimmune disease? / Flodström, M.; Shi, F. D.; Sarvetnick, Nora E; Ljunggren, H. G.

In: Scandinavian Journal of Immunology, Vol. 55, No. 5, 08.05.2002, p. 432-441.

Research output: Contribution to journalReview article

Flodström, M. ; Shi, F. D. ; Sarvetnick, Nora E ; Ljunggren, H. G. / The natural killer cell - Friend or foe in autoimmune disease?. In: Scandinavian Journal of Immunology. 2002 ; Vol. 55, No. 5. pp. 432-441.
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