Mesangial Cells Exhibit Features of Antigen-Presenting Cells and Activate CD4+ T Cell Responses

Yu, Hongyu; Cui, Shaoyuan; Mei, Yan; Li, Qinggang; Wu, Lingling; Duan, Shuwei; Cai, Guangyan; Zhu, Hanyu; Fu, Bo; Zhang, Li; Feng, Zhe; Chen, Xiangmei

doi:10.1155/2019/2121849

Cited by 20 publications

(18 citation statements)

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“…Moreover, the activated cDCs with tRA pre-treatment may have directly contributed to the activation of mesangial cells in the kidney through producing an array of pro-inflammatory cytokines and chemokines (84)(85)(86)(87)(88). Recent findings by Yu et al (89) provide support for our explanation that the potentiation of mesangial cell activity by tRA pre-treatment contributes to exacerbation of pristane-induced glomerulonephritis. They found that in vitro-activated mesangial cells could act as nonprofessional antigen-presenting cells and express cell surface molecules associated with antigen presentation including MHC-II, ICAM-1, CD40, and CD80, and therefore were able to prime co-cultured T cells to promote their activation and polarization toward T helper-1 (Th1) cells (89).…”

Section: Discussionsupporting

confidence: 80%

“…Recent findings by Yu et al (89) provide support for our explanation that the potentiation of mesangial cell activity by tRA pre-treatment contributes to exacerbation of pristane-induced glomerulonephritis. They found that in vitro-activated mesangial cells could act as nonprofessional antigen-presenting cells and express cell surface molecules associated with antigen presentation including MHC-II, ICAM-1, CD40, and CD80, and therefore were able to prime co-cultured T cells to promote their activation and polarization toward T helper-1 (Th1) cells (89). It is likely that the combination of pristane and tRA pre-treatment creates a favorable cytokine/chemokine environment for mesangial cell proliferation, whereas the proliferating mesangial cells would acquire abilities to present antigens, thereby promoting Th1 differentiation and renal inflammation.…”

Section: Discussionsupporting

confidence: 80%

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Retinoic Acid Exerts Disease Stage-Dependent Effects on Pristane-Induced Lupus

et al. 2020

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We previously showed that all-trans-retinoic acid (tRA), an active metabolite of vitamin A, exacerbated pre-existing autoimmunity in lupus; however, its effects before the development of autoimmunity are unknown. Here, using a pristane-induced model, we show that tRA exerts differential effects when given at the initiation vs. continuation phase of lupus. Unlike tRA treatment during active disease, pre-pristane treatment with tRA aggravated glomerulonephritis through increasing renal expression of pro-fibrotic protein laminin β1, activating bone marrow conventional dendritic cells (cDCs), and upregulating the interaction of ICAM-1 and LFA-1 in the spleen, indicating an active process of leukocyte activation and trafficking. Transcriptomic analysis revealed that prior to lupus induction, tRA significantly upregulated the expression of genes associated with cDC activation and migration. Post-pristane tRA treatment, on the other hand, did not significantly alter the severity of glomerulonephritis; rather, it exerted immunosuppressive functions of decreasing circulatory and renal deposition of autoantibodies as well as suppressing the renal expression of proinflammatory cytokines and chemokines. Together, these findings suggest that tRA differentially modulate lupus-associated kidney inflammation depending on the time of administration. Interestingly, both pre-and post-pristane treatments with tRA reversed pristane-induced leaky gut and modulated the gut microbiota in a similar fashion, suggesting a gut microbiota-independent mechanism by which tRA affects the initiation vs. continuation phase of lupus.

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Section: Discussionsupporting

confidence: 80%

Section: Discussionsupporting

confidence: 80%

Retinoic Acid Exerts Disease Stage-Dependent Effects on Pristane-Induced Lupus

et al. 2020

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“…Once differentiated, Th17 cells secrete their cytokines (IL-17A, IL-17F, IL-17C, IL-21, and IL-22), most of them with a pathogenic role in the kidney (32, 86-88), in addition to its systemic effects (1,15). Regarding Th17 cells differentiation, it is also worth mentioning that podocytes, mesangial cells, and renal tubular epithelial cells can behave as antigen-presenting cells (89)(90)(91)(92). So, these intrinsic renal cells can alone trigger the local activation of Th17 cells after recognizing, processing, presenting eventual DAMPs that cross the glomerular filtration barrier, as seen in other kidney disease models (89,93,94).…”

Section: Activation and Differentiation Of Th17 Cellsmentioning

confidence: 99%

The Th17/IL-17 Axis and Kidney Diseases, With Focus on Lupus Nephritis

Paquissi

Abensur

2021

Front. Med.

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Systemic lupus erythematosus (SLE) is a disease characterized by dysregulation and hyperreactivity of the immune response at various levels, including hyperactivation of effector cell subtypes, autoantibodies production, immune complex formation, and deposition in tissues. The consequences of hyperreactivity to the self are systemic and local inflammation and tissue damage in multiple organs. Lupus nephritis (LN) is one of the most worrying manifestations of SLE, and most patients have this involvement at some point in the course of the disease. Among the effector cells involved, the Th17, a subtype of T helper cells (CD4+), has shown significant hyperactivation and participates in kidney damage and many other organs. Th17 cells have IL-17A and IL-17F as main cytokines with receptors expressed in most renal cells, being involved in the activation of many proinflammatory and profibrotic pathways. The Th17/IL-17 axis promotes and maintains repetitive tissue damage and maladaptive repair; leading to fibrosis, loss of organ architecture and function. In the podocytes, the Th17/IL-17 axis effects include changes of the cytoskeleton with increased motility, decreased expression of health proteins, increased oxidative stress, and activation of the inflammasome and caspases resulting in podocytes apoptosis. In renal tubular epithelial cells, the Th17/IL-17 axis promotes the activation of profibrotic pathways such as increased TGF-β expression and epithelial-mesenchymal transition (EMT) with consequent increase of extracellular matrix proteins. In addition, the IL-17 promotes a proinflammatory environment by stimulating the synthesis of inflammatory cytokines by intrinsic renal cells and immune cells, and the synthesis of growth factors and chemokines, which together result in granulopoiesis/myelopoiesis, and further recruitment of immune cells to the kidney. The purpose of this work is to present the prognostic and immunopathologic role of the Th17/IL-17 axis in Kidney diseases, with a special focus on LN, including its exploration as a potential immunotherapeutic target in this complication.

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“…The multifunctional cytokine IL-10 is primarily produced by stimulated T cells and suppresses strong inflammatory reactions [ 35 , 36 ]. Marconi et al [ 37 ], in their research with human serum, demonstrated that, together with IL-4, it induced IgA production, which is in line with our studies.…”

Section: Discussionmentioning

confidence: 99%

OVA-Experienced CD4+ T Cell Transfer and Chicken Protein Challenge Affect the Immune Response to OVA in a Murine Model

Fuc

Złotkowska

Wasilewska

et al. 2021

IJMS

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Chicken meat is often a major component of a modern diet. Allergy to chicken meat is relatively rare and occurs independently or in subjects allergic to ovalbumin (OVA). We examined the effect of adoptive transfer of OVA-CD4+ T cells on the immune response to OVA in mice fed chicken meat. Donor mice were injected intraperitoneally with 100 µg of OVA with Freund’s adjuvant two times over a week, and CD4+ T cells were isolated from them and transferred to naïve mice (CD4+/OVA/ChM group), which were then provoked with OVA with FA and fed freeze-dried chicken meat for 14 days. The mice injected with OVA and fed chicken meat (OVA/ChM group), and sensitized (OVA group) and healthy (PBS group) mice served as controls. Humoral and cellular response to OVA was monitored over the study. The CD4+/OVA/ChM group had lowered levels of anti-OVA IgG and IgA, and total IgE. There were significant differences in CD4+, CD4+CD25+, and CD4+CD25+Foxp3+ T cells between groups. OVA stimulation decreased the splenocyte proliferation index and IFN-γ secretion in the CD4+/OVA/ChM group compared to the OVA group. IL-4 was increased in the OVA/ChM mice, which confirms allergenic potential of the egg–meat protein combination. Transfer of OVA-experienced CD4+ T cells ameliorated the negative immune response to OVA.

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Mesangial Cells Exhibit Features of Antigen-Presenting Cells and Activate CD4+ T Cell Responses

Cited by 20 publications

References 50 publications

Retinoic Acid Exerts Disease Stage-Dependent Effects on Pristane-Induced Lupus

Retinoic Acid Exerts Disease Stage-Dependent Effects on Pristane-Induced Lupus

The Th17/IL-17 Axis and Kidney Diseases, With Focus on Lupus Nephritis

OVA-Experienced CD4+ T Cell Transfer and Chicken Protein Challenge Affect the Immune Response to OVA in a Murine Model

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