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J Immunol. 2016 Oct 1;197(7):2618-26. doi: 10.4049/jimmunol.1401129. Epub 2016 Aug 24.

Selective Memory to Apoptotic Cell-Derived Self-Antigens with Implications for Systemic Lupus Erythematosus Development.

Author information

1
Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, 171 77 Stockholm, Sweden;
2
Department of Medicine, Karolinska Institutet, 171 77 Stockholm, Sweden; and.
3
Princess Margaret Cancer Centre, University Health Network, Toronto, Ontario M5G 2M9, Canada.
4
Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, 171 77 Stockholm, Sweden; mikael.karlsson@ki.se.

Abstract

Autoimmune diseases are characterized by pathogenic immune responses to self-antigens. In systemic lupus erythematosus (SLE), many self-antigens are found in apoptotic cells (ACs), and defects in removal of ACs from the body are linked to a risk for developing SLE. This includes pathological memory that gives rise to disease flares. In this study, we investigated how memory to AC-derived self-antigens develops and the contribution of self-memory to the development of lupus-related pathology. Multiple injections of ACs without adjuvant into wild-type mice induce a transient primary autoimmune response without apparent anti-nuclear Ab reactivity or kidney pathology. Interestingly, as the transient Ab response reached baseline, a single boost injection fully recalled the immune response to ACs, and this memory response was furthermore transferable into naive mice. Additionally, the memory response contains elements of pathogenicity, accompanied by selective memory to selective Ags. Thus, we provide evidence for a selective self-memory that underlies progression of the response to self-antigens with implications for SLE development therapy.

Comment in

PMID:
27559051
PMCID:
PMC5026029
DOI:
10.4049/jimmunol.1401129
[Indexed for MEDLINE]
Free PMC Article

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