The decreased of peripheral blood natural killer cell is associated with serum IL-2 level in the renal tubular acidosis in patients with primary sjogren’s syndrome

Abstract

Background Primary Sjogren’s Syndrome (pSS) is a lymphoproliferative disease with autoimmune characteristics, which is characterized by lymphocyte infiltration of exocrine glands and involvement and dysfunction of extraglandular organs. Renal tubular acidosis (RTA) is a common renal involvement in pSS. This study investigated the phenotypic characteristics of peripheral blood lymphocyte subsets and cytokines in pSS patients complicated with RTA (pSS-RTA). Method This retrospective study included 25 pSS patients complicated with RTA and 54 pSS patients without RTA (pSS-no-RTA). To examine the level of peripheral lymphocytes subsets, flow cytometry analysis was used. The level of serum cytokines were detected by flow cytometry bead array(CBA). The influencing factors related to the occurrence of pSS-RTA were identified through logistic regression analyze. Results The absolute number of CD4 + T cells and Th2 cells in peripheral blood were decreased in pSS-RTA patients than pSS-no-RTA patients. Moreover, the absolute number of NK cells and Treg cells were also decreased in pSS-RTA patients than pSS-no-RTA. The level of serum IL-2 was higher in pSS-RTA patients than pSS-no-RTA patients, and is negatively correlated with the number of NK cells, the number and percentage of Th17 cells, and Th17/Treg. Serum IL-2 level is also correlated with various cytokines. Multivariate logistic analysis proved that elevated ESR and ALP were risk factors for pSS complicated with RTA, while Treg was a protective factor. Conclusion The increase of serum IL-2 level and the decrease of peripheral blood NK cells and Treg cells may be the immune mechanism of the development of pSS-RTA disease.

The proportion of CD161 on CD56+ NK cells in peripheral circulation associates with clinical features and disease activity of primary Sjögren's syndrome

“…6 Another study found that the absolute number of NK cells in pSS patients with renal tubular acidosis (RTA) was significantly lower than that in patients without RTA. 4 The above studies indicate that NK cells are involved in the disease development of pSS. Similarly, previous studies found that NK cells in peripheral circulation decreased in SSc, especially in patients with organ involvement, and speculated that the decrease of NK cell proportion in peripheral blood may be due to the infiltration of NK cells into the involved tissues.…”

“…It was speculated that the reduction of NK cells in the peripheral blood of pSS patients may be due to the augmented homing of cytotoxic cells to exocrine glands, which trigger and maintain tissue inflammation by producing Th1 cytokines and cytotoxic mediators 6 . Another study found that the absolute number of NK cells in pSS patients with renal tubular acidosis (RTA) was significantly lower than that in patients without RTA 4 . The above studies indicate that NK cells are involved in the disease development of pSS.…”

“…3 Recent studies have found that the expression of NK cells in peripheral blood or salivary glands of pSS patients or model mice was abnormal, which was related to the activity and severity of the disease. [4][5][6] CD161 is one of the members of human NKRP1 subfamily, which is called NK cell receptor protein 1A (NKR-P1A) or killer cell lectin-like receptor subfamily B member 1 (KLRB1), and it is also a type II transmembrane C-type lectin glycoprotein receptor, which is called C-type lectin domain family 5 member B (CLEC5B). 7 CD161 is mostly expressed in NK cells and T cell subsets such as CD4 + T cells, CD8 αβT cells, γδT cells, and NKT cells.…”

“…It is well known that pSS is mainly mediated by T cells and B cells, but innate immune cells such as NK cells also play an important role in the pathogenesis of pSS 3 . Recent studies have found that the expression of NK cells in peripheral blood or salivary glands of pSS patients or model mice was abnormal, which was related to the activity and severity of the disease 4–6 …”