These cells had enhanced immunosuppression <i>in vitro</i> in terms of inhibiting splenocyte proliferation, reducing proinflammatory factors (IL-1<i>β</i>, TNF-<i>α</i>, IL-17, and IL-6), and suppressing autoantibodies (anti-dsDNA and anti-ANA).
Here, we show that combining low doses of IL-2 cplxs with rapamycin and blockade of the inflammatory cytokine IL-6 leads to long-term (>75 d) survival of major histocompatibility complex-different skin allografts without the need for immunosuppression.
Systemic inflammation as measured by serum IL-6 is associated with an increased risk of advanced immunosuppression, all-cause mortality, HAND, and depression but not neuropathy or headaches among ART-naïve HIV+ adults in rural Uganda.
IL-6 plays a role in cancer pathogenesis via its connection to proteins involved in the formation of desmoplastic stroma and to immunosuppression by driving differentiation of myeloid suppressor cells together with TGF-β.
GIPS significantly raised the serum levels of immunoglobulin (Ig)A and IgG, promoted the production of interleukins (ILs), including IL-2, IL-3 and IL-6, interferons, including interferon (IFN)-α and IFN-γ, and monocyte chemotactic protein 1 in the spleen, which resulted in accelerating recovery of immunosuppression.
CONCLUSIONS Our study indicates that IL-6 induces strong immunosuppression in the CRC microenvironment by recruiting immunosuppression cells and impairing T cell infiltration.
IL-6 blockade abrogated the obesity-induced resistance to anti-VEGF therapy in primary and metastatic sites by directly affecting tumor cell proliferation, normalizing tumor vasculature, alleviating hypoxia, and reducing immunosuppression.
Expression of the anti-inflammatory cytokine IL-10 was increased in endometrial tissues, while expression of the pro-inflammatory cytokine IL-6 was decreased, indicating immunosuppression.
High IL-6 expression CAFs could induce strong immunosuppression in HCC microenvironment by recruiting immunosuppressive cells, such as myeloid derived suppressive cells.
Pharmacological inhibition of prostaglandin E2 (PGE2) synthesis and, in some MSCs, interleukin-6 (IL-6) activity restored NK function, whereas NK cell stimulation by PGE2 alone mimicked T-MSC-mediated immunosuppression.
Autophagy inhibition by 3-methyladenine obviously aggravates this morphine-induced memory impairment, accompanied with increased cell deaths in stratum pyramidale of hippocampal CA1, CA3, and DG regions and the activation of microglia to induce inflammation in hippocampus, such as upregulated expression of TNF-α, IL-1β, IL-6, and iNOS, as well as NF-κB' s activation, while morphine alone promoted microglial immunosuppression in hippocampus with autophagy activation which was also confirmed in primary microglia.
Increased activation of the IL-6 pathway observed in our cells might represent an adaptive mechanism to senescence, but preserving some specific cellular functions, including immunosuppression.
Compared with HCs, BK-negative patients had lower urine sIL-1RA (P=0.003), sIL-6R (P=0.001), and IL-17 (P<0.001), whereas BK-positive patients had higher urine IL-3 (P=0.004) and IL-6 (P=0.001) and lower IL-17 (P<0.001), suggesting cytokine suppression by immunosuppression and upregulation by BK-infection.
In plasma, high levels of interleukin-6 could be detected by an enzyme-linked immunosorbent assay system, with rapid decline correlating with immunosuppression and improving clinical course.