American Journal of BioScience
Volume 7, Issue 2, March 2019, Pages: 50-57
Received: Aug. 26, 2019;
Published: Sep. 27, 2019
Views 135 Downloads 25
Zhi Xiao, Department of Nephrology, Binzhou People's Hospital, Binzhou City, P. R. China
Binbin Wang, Emergency Department, Binzhou People's Hospital, Binzhou City, P. R. China
Shufang Li, Department of Respiratory, Binzhou People's Hospital, Binzhou City, P. R. China
Objective to discuss the possible role and mechanism of DCs in IgAN attack. Method Stimulating factors such as recombinant human granulocyte-macrophage colony stimulating factor (rhGM-CSF), recombinant human interleukin-4 (rhIL-4) and tumor necrosis factor-a (TNF-a) etc. were used in vitro jointly to induce and culture DCs, a flow cytometry was used to detect expression of HLA-DR, CD83 and CDla of DCs membrane surface molecules, the MTT method was used to detect capacity of DCs of the IgAN patient group to stimulate proliferation of allogeneic T cells and the difference between the levels of interleukin 6 (IL-6) and interleukin 12 (IL-12) secreted by DCs and that of the normal control group. Result Combined application of cytokines GM-CSF, IL-4 and TNF-a is able to induce proliferation and differentiation of peripheral blood mononuclear cell into a mature dendritic cell. The surface of mature dendritic cells highly expresses human leucocyte antigen HLA-DR and surface maturity markers of relative specificity of dendritic cells, CD83 and CD1a. The capacity of DCs of the IgAN patient group to stimulate allogeneic T lymphocyte proliferation is higher than that of the normal control group and the difference has statistical significance (P<0.05). The capacity of DCs of the patient group influenced by lipopolysaccharide (LPS) to stimulate allogeneic T lymphocyte proliferation significantly increases compared with that of DCs of the patient group not influenced by lipopolysaccharide (LPS) and the difference has statistical significance (P<0.05). The IL-6 secreted by the DCs of the IgAN patient group is higher than that of the normal control group and the difference between the two groups has statistical significance (P<0.05). The IL-12 secreted by the DCs of the IgAN patient group is lower than that of the normal control group and the difference between the two groups has statistical significance (P<0.05). Conclusion DCs may regulate the balance between Thl/Th2 cells by secreting cytokines so as to play an imporat role in occurence and progression of IgAN and such factors as infection etc. may strengthen the functions of DCs thus easily triggering IgAN.
Role of Dendrtic Cells in IgA Nephropathy Pathogenesis, American Journal of BioScience.
Vol. 7, No. 2,
2019, pp. 50-57.
Kajiyama T. Suzuki Y. et al. Different pathological roles of toll-like receptor 9 on mucosal B cells and dendritic cells in murine IgA nephropathy [J]. Clin Dev Immunol, 2011, 37 (9): 646-8.
Tezuka H. Abe Y. et al. Prominent role for plasmacytoid dendritic cells in mucosal T cell-independent IgA induction [J]. Immunity, 2011, 34 (2): 247-57.
Eijgenraam JW. Reinartz SM. et al. Immuno-histological analysis of dendritic cells in nasal biopsies of IgA nephropathy patients [J]. Nephrol Dial Transplant, 2008, 23 (2): 612-20.
Okusa MD. Li L. Dendritic cells in acute kidney injury: cues from the microenvironment [J]. Trans Am Clin Climatol Assoc, 2012, 123: 54-62.
Li L. Huang L. et al. Dendritic cells tolerized with adenosine A (2) AR agonist attenuate acute kidney injury [J]. J Clin Invest, 2012, 122 (11): 3931-42.
Zheng D. Cao Q. et al. Lipopolysaccharide-pretreated plasmacytoid dendritic cells ameliorate experimental chronic kidney disease [J]. Kidney Int, 2012, 81 (9): 892-902.
Lu L. Faubel S. et al. Depletion of macrophages and dendritic cells in ischemic acute kidney injury [J]. Am J Nephrol, 2012, 35 (2): 181-90.
Huang Y. Johnston P. et al. Kidney-derived stromal cells modulate dendritic and T cell responses [J]. J Am Soc Nephrol, 2009, 20 (4): 831-41.
Carney EF. Acute kidney injury: Adoptive transfer of tolerized dendritic cells--a potential new strategy for the prevention of AKI [J]. Nat Rev Nephrol, 2013, 9 (1): 4-5.
Takahashi E. Kataoka K. et al. Oral clarithromycin enhances airway immunoglobulin A (IgA) immunity through induction of IgA class switching recombination and B-cell-activating factor of the tumor necrosis factor family molecule on mucosal dendritic cells in mice infected with influenza A virus [J]. J Virol, 2012, 86 (20): 10924-34.
Suzuki Y. Suda T. et al. Mouse CD11bhigh lung dendritic cells have more potent capability to induce IgA than CD103+ lung dendritic cells in vitro [J]. Am J Respir Cell Mol Biol, 2012, 46 (6): 773-80.
Fukuyama Y. Tokuhara D. et al. Potential roles of CCR5 (+) CCR6 (+) dendritic cells induced by nasal ovalbumin plus Flt3 ligand expressing adenovirus for mucosal IgA responses [J]. PLoS One, 2013, 8 (4): 453-5.
Endsley MA. Njongmeta LM. et al. Human IgA-inducing protein from dendritic cells induces IgA production by naive IgD+ B cells [J]. J Immunol, 2009, 182 (4): 1854-9.
Machida Y. Kitamoto K. et al. Renal fibrosis in murine obstructive nephropathy is attenuated by depletion of monocyte lineage, not dendritic cells [J]. J Pharmacol, 2010, 114 (4): 464-73.
Kataoka K. Fujihashi K. et al. Oral-nasopharyngeal dendritic cells mediate T cell-independent IgA class switching on B-1 B cells [J]. PLoS One, 2011, 6 (9): 396-8.
Wang T. Xu L. et al. Immature CD4 (+) dendritic cells conditioned with donor kidney antigen prolong renal allograft survival in rats [J]. Chin Med J (Engl), 2012, 125 (14): 2530-7.
Gloudemans AK. Plantinga M. et al. The mucosal adjuvant cholera toxin B instructs non-mucosal dendritic cells to promote IgA production via retinoic acid and TGF-beta [J]. PLoS One, 2013, 8 (3): 822-4.
Flores-Langarica A. Marshall JL. et al. Systemic flagellin immunization stimulates mucosal CD103+ dendritic cells and drives Foxp3+ regulatory T cell and IgA responses in the mesenteric lymph node [J]. J Immunol, 2012, 189 (12): 5745-54.
Ye C. Bhan A. et al. Silencing TNF-alpha in macrophages and dendritic cells for arthritis treatment [J]. Scand J Rheumatol, 2013, 13 (6): 152-3.
Gasparini C. Foxwell BM. et al. RelB/p50 regulates TNF production in LPS-stimulated dendritic cells and macrophages [J]. Cytokine, 2013, 61 (3): 736-40.
Dong X. Bachman LA. et al. Dendritic cells facilitate accumulation of IL-17 T cells in the kidney following acute renal obstruction [J]. Kidney Int, 2008, 74 (10): 1294-309.
Rees A. Cross dendritic cells anger T cells after kidney injury [J]. J Am Soc Nephrol, 2009, 20 (1): 3-5.
Miwa S. Nishida H. et al. TNF-alpha and tumor lysate promote the maturation of dendritic cells for immunotherapy for advanced malignant bone and soft tissue tumors [J]. PLoS One, 2012, 7 (12): 926-7.
Munich S. Sobo-Vujanovic A. et al. Dendritic cell exosomes directly kill tumor cells and activate natural killer cells via TNF superfamily ligands [J]. Oncoimmunology, 2012, 1 (7): 1074-1083.
Bessa J. Jegerlehner A. et al. Alveolar macrophages and lung dendritic cells sense RNA and drive mucosal IgA responses [J]. J Immunol, 2009, 183 (6): 3788-99.
Tittel AP. Heuser C. et al. Kidney dendritic cells induce innate immunity against bacterial pyelonephritis [J]. J Am Soc Nephrol, 2011, 22 (8): 1435-41.
Stax AM. Gelderman KA. et al. Induction of donor-specific T-cell hyporesponsiveness using dexamethasone-treated dendritic cells in two fully mismatched rat kidney transplantation models [J]. Transplantation, 2008, 86 (9): 1275-82.
Shi B. Ren G. et al. HBsAg inhibits IFN-alpha production in plasmacytoid dendritic cells through TNF-alpha and IL-10 induction in monocytes [J]. PLoS One, 2012, 7 (9): 900-3.
Yi HJ. Lu GX. Adherent and non-adherent dendritic cells are equivalently qualified in GM-CSF, IL-4 and TNF-alpha culture system [J]. Cell Immunol, 2012, 277 (2): 44-8.
Lehner M. Kellert B. et al. Autocrine TNF is critical for the survival of human dendritic cells by regulating BAK, BCL-2, and FLIPL [J]. J Immunol, 2012, 188 (10): 4810-8.