Abstract
BackgroundInnate lymphoid cells (ILCs) play an essential role in maintaining homeostasis; however, they can also cause chronic inflammation and autoimmune disease. This study aimed to identify the role of ILCs in the pathogenesis of lupus nephritis (LN).MethodsThe percentage of ILCs within the peripheral blood mononuclear cell (PBMC) population and urine of patients with LN (n = 16), healthy controls (HC; n = 8), and disease controls (ANCA-associated vasculitis (AAV; n = 6), IgA nephropathy (IgAN; n = 9), and other glomerular diseases (n = 5)) was determined by flow cytometry analysis. In addition, ILCs were sorted and cultured with plasma from LN patients or HC to elucidate whether the reduced population of CD117+ ILCs observed in LN was due to changes in the ILC progenitor population.ResultsThe percentage of total ILCs and CD117+ ILCs in LN was significantly lower than that in HC. The percentage of cytokine-secreting ILCs was also lower in LN; however, when the disease stabilized, cytokine production was restored to levels similar to those in HC. The increase in the number of exhausted ILCs (cells unable to secrete cytokines) correlated positively with disease activity. When CD117+ ILCs were cultured with LN plasma, the number of CD117+ ILCs fell, but that of other ILC subsets increased.ConclusionsThe percentage of CD117+ ILCs and the capacity of ILCs to secrete cytokines fell as LN severity increased, suggesting that an inflammatory environment of LN induces persistent differentiation and exhaustion of ILCs.
Highlights
Lupus nephritis (LN) is a renal inflammation caused by systemic lupus erythematosus (SLE)
These Innate lymphoid cell (ILC) were further subdivided according to the expression of surface markers; CRTH2 for ILC2s, CD117 for ILC3s and/or progenitor of ILCs, and CRTH2−/CD117− for ILC1s (Fig. 1a, b)
We noted that CD117+ ILCs in most patients with autoimmune kidney diseases showed reduced numbers (LN (P = 0.0003), ANCA-associated vasculitis (AAV) (P = 0.0877), and IgA nephropathy (IgAN) (P = 0.0014)), but not in Minimal change disease (MCD) or Focal segmental glomerulosclerosis (FSGS)
Summary
Lupus nephritis (LN) is a renal inflammation caused by systemic lupus erythematosus (SLE). Innate lymphoid cells (ILCs) are a newly discovered type of immune cell that is characterized by antigenindependent activation. They do not react in an antigen-specific manner, ILCs resemble T cells in that they share key transcription factors and produce cytokines. Group 1 ILCs (ILC1s) including NK cells express T-bet and produce IFN-γ and TNF-α. Group 2 ILCs (ILC2s) express GATA3 and produce mainly type 2 cytokines such as IL-5 and IL-13. Human and mouse ILCs are classified according to the expression of surface markers; Lin− (Lineage (Lin) markers; a collection of surface markers of immune cells, not those of ILCs) CD127+ lymphocytes. Innate lymphoid cells (ILCs) play an essential role in maintaining homeostasis; they can cause chronic inflammation and autoimmune disease. This study aimed to identify the role of ILCs in the pathogenesis of lupus nephritis (LN)
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