Inhibition of the type I immune responses of human monocytes by IFN-α and IFN-β

Paus, Roelof A. de; Wengen, Annelies van; Schmidt, Iris; Visser, Marten; Verdegaal, Els M.E.; Dissel, Jaap T. van; Vosse, Esther van de

doi:10.1016/j.cyto.2012.12.005

Cited by 57 publications

(58 citation statements)

References 33 publications

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“…S9E). Type I IFNs are known to inhibit IL-12-p70 in myeloid cells, including DCs (27), and in particular in M. tuberculosis-infected monocytes and macrophages (28,29). Accordingly, stimulation by IFNβ resulted in a strong suppression of IL-12-p70 production by TLR2-activated In I, cells were left untreated or were treated with the SHP2 inhibitor GS-493 (24).…”

Section: Dcir Deficiency Results In Enhanced Antimycobacterial Th1 Immentioning

confidence: 99%

C-type lectin receptor DCIR modulates immunity to tuberculosis by sustaining type I interferon signaling in dendritic cells

Troegeler

Mercier

Cougoule

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

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Immune response against pathogens is a tightly regulated process that must ensure microbial control while preserving integrity of the infected organs. Tuberculosis (TB) is a paramount example of a chronic infection in which antimicrobial immunity is protective in the vast majority of infected individuals but can become detrimental if not finely tuned. Here, we report that C-type lectin dendritic cell (DC) immunoreceptor (DCIR), a key component in DC homeostasis, is required to modulate lung inflammation and bacterial burden in TB. DCIR is abundantly expressed in pulmonary lesions in Mycobacterium tuberculosis-infected nonhuman primates during both latent and active disease. In mice, we found that DCIR deficiency impairs STAT1-mediated type I IFN signaling in DCs, leading to increased production of IL-12 and increased differentiation of T lymphocytes toward Th1 during infection. As a consequence, DCIR-deficient mice control M. tuberculosis better than WT animals but also develop more inflammation characterized by an increased production of TNF and inducible NOS (iNOS) in the lungs. Altogether, our results reveal a pathway by which a C-type lectin modulates the equilibrium between infection-driven inflammation and pathogen’s control through sustaining type I IFN signaling in DCs.

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Section: Dcir Deficiency Results In Enhanced Antimycobacterial Th1 Immentioning

confidence: 99%

C-type lectin receptor DCIR modulates immunity to tuberculosis by sustaining type I interferon signaling in dendritic cells

Troegeler

Mercier

Cougoule

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

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“…It is possible that IFN-γ is not the only cytokine with a role in the TB microenvironment, other cytokines, such as IFN-α, may also have an effect (26,36). In a previous study it was reported that IFN-α and IFN-β strongly inhibited IFN-γ responsiveness and the production of type I cytokines (15); however, no differences in IFN-α levels were detected in the TPE, MPE and n-TB n-M groups in the present study.…”

Section: A B Cmentioning

confidence: 99%

“…sPD-L1 was initially identified in the blood serum of patients with non-small cell lung cancer, and increased sPD-L1 expression is associated with lung cancer TNM staging and the patient's clinical response to treatment (12). Increased levels of serum sPD-L1 have also been detected in other solid tumors, such as aggressive renal cell carcinoma, breast cancer and autoimmune diseases, including systemic lupus erythematosus, rheumatoid arthritis and type 2 diabetes mellitus (13)(14)(15)(16). Therefore, sPD-L1 may have important roles in the regulation of co-stimulatory signals.…”

Section: Introductionmentioning

confidence: 99%

Increased soluble and membrane-bound PD-L1 contributes to immune regulation and disease progression in patients with tuberculous pleural effusion

Pan

Zhong

Xing

et al. 2016

Experimental and Therapeutic Medicine

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Abstract. Soluble and membrane-bound programmed death ligand-1 (sPD-L1 and mPD-L1, respectively) have been demonstrated to participate in the immune suppression of non-small cell lung cancer. However, the contribution of sPD-L1 and mPD-L1 to immune regulation and disease progression in patients with pleural effusions remains unknown. The present study evaluated the levels of sPD-L1 and membrane-bound PD-1/PD-L1 in the peripheral blood and pleural effusions of patients with tuberculous pleural effusion (TPE), malignant pleural effusion (MPE) and non-tuberculous non-malignant pleural effusion (n-TB n-M). Furthermore, selected T lymphocytes and cluster of differentiation (CD)14 + monocytes were co-cultured to investigate the potential effect of the PD-1/PD-L1 pathway in TPE. Levels of sPD-L1 and PD-L1 on CD14 + monocytes were increased in the TPE group, as compared with the MPE and n-TB n-M groups. Furthermore, sPD-L1 levels and the expression levels of PD-L1 on CD14 + monocytes were demonstrated to be positively correlated with interferon (IFN)-γ concentration in pleural effusions. Therefore, IFN-γ may increase the expression of PD-L1 on CD14 + monocytes in vitro. Cell counting kit-8 analysis demonstrated that anti-PD-L1 antibody was able to partially reverse the proliferation of T lymphocytes in the co-culture system. The results of the present study indicated that sPD-L1 or mPD-L1 are associated with the immune regulation and disease progression of TPE, and may serve as possible biomarkers of TPE. Furthermore, sPD-L1 and the PD-1/PD-L1 pathway of TPE may be associated with the Th1 immune response; therefore, an anti-PD-1/PD-L1 pathway suggests a potential immune therapy strategy for the treatment of TPE.

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“…Integration of the training cohort from this study The common IFN-b/IL-10 signature was present even though (i) one study involved leprosy and two studies involved TB, (ii) one study involved skin lesions and two studies involved peripheral blood, (iii) the comparisons in each case were two different control groups, and (iv) all three studies used different microarray platforms. In addition, type I IFNs have been shown to contribute to disease susceptibility in TB by cross-regulating induction of IL-1 (167, 168) and blocking IFN-g-induced cytokine responses in monocytes (169). The data strongly indicate that a common IFN-b-inducible gene program correlates with extent of disease in both leprosy and TB, suggesting that IFN-b, through mediation by IL-10, is a common factor contributing to pathogenesis in the two distinct mycobacterial diseases.…”

Section: Learning From Leprosymentioning

confidence: 99%