Human sCD14 ELISA kit

Psoriasis is a chronic autoimmune disease. Identification of the biomarkers responsible for Traditional Chinese Medicine (TCM) syndromes of psoriasis can help researchers recognize the different aspects of psoriasis and find novel therapeutic targets for the treatment of psoriasis. The current study investigated the levels of circulating Mo-MDSCs and Mo-MDSC-associated immune factors in the peripheral blood of psoriasis patients with different TCM syndromes. We found that the frequency of Mo-MDSCs (CD14(+)HLA-DR-/low cells) among CD14(+) cells from plaque psoriasis patients with blood-stasis (BS) syndrome was significantly increased when compared with healthy controls mml:mfenced close=")" open="(" separators="|"p<0.001 and blood-heat (BH) syndrome group mml:mfenced close=")" open="(" separators="|"p<0.001, respectively. However, serum IL-2, IL-4, IL-6, IL-10, IL-17A, TNF-alpha, IFN-gamma, iNOS, Arg-1, and NO concentration showed no statistically significant difference between healthy controls and psoriasis patients as well as no significant difference between the BH and BS syndrome groups. Compared with healthy controls, the mRNA expression of Arg-1, TNF-alpha, ROR-gamma, and PD-L1 was increased, while the mRNA expression of PD-1 and IL-10 was decreased in PBMCs from psoriasis patients. Moreover, the mRNA expression of TNF-alpha and FOXP3 in PBMCs showed a pronounced statistical difference between the psoriatic BH syndrome group and the BS syndrome group. Therefore, we provide evidence that the percentage of CD14(+)HLA-DR-/low MDSC/ CD14(+) cells and TNF-alpha and Foxp3 mRNA expression levels in PBMCs are potential biomarkers for distinguishing TCM BH syndrome and BS syndrome.

Systemic sclerosis (SSc) is a T helper type 2 (Th2)-associated autoimmune disease characterized by vasculopathy and fibrosis. Efficacy of B cell depletion therapy underscores antibody-independent functions of B cells in SSc. A recent study showed that the Th2 cytokine interleukin (IL)-4 induces granulocyte-macrophage colony-stimulating factor (GM-CSF)-producing effector B cells (GM-B-effs) in humans. In this study, we sought to elucidate the generation mechanism of GM-B(effs)and also determine a role of this subset in SSc. Among Th-associated cytokines, IL-4 most significantly facilitated the generation of GM-B(effs)within memory B cells in healthy controls (HCs). In addition, the profibrotic cytokine transforming growth factor (TGF)-beta further potentiated IL-4- and IL-13-induced GM-B-effs. Of note, tofacitinib, a Janus kinase (JAK) inhibitor, inhibited the expression of GM-CSF mRNA and protein in memory B cells induced by IL-4, but not by TGF-beta. GM-B(effs)were enriched within CD20(+)CD30(+)CD38(-/low)cells, a distinct population from plasmablasts, suggesting that GM-B(effs)exert antibody-independent functions. GM-B(effs)were also enriched in a CD30(+)fraction of freshly isolated B cells. GM-B(effs)generated under Th2 conditions facilitated the differentiation from CD14(+)monocytes to DC-SIGN(+)CD1a(+)CD14(-)CD86(+)cells, which significantly promoted the proliferation of naive T cells. CD30(+)GM-B(effs)were more pronounced in patients with SSc than in HCs. A subpopulation of SSc patients with the diffuse type and concomitant interstitial lung disease exhibited high numbers of GM-B-effs. Together, these findings suggest that human GM-B(effs)are enriched in a CD30(+)B cell subset and play a role in the pathogenesis of SSc.