Abstract Immunoglobulin A (IgA) vasculitis is the most common leukocytoclastic small-vessel vasculitis in children and mainly involves the small vessels in the skin, joints, digestive tract, and kidneys. Its pathogenesis is still unclear. Currently, it is believed that environmental factors can cause autoimmune dysfunction and lead to the deposition of IgA-containing immune complexes on the wall of arterioles on the basis of genetic factors. This article reviews the research advances in the role of immune factors in the pathogenesis of IgA vasculitis.
Piram M, Mahr A. Epidemiology of immunoglobulin A vasculitis (Henoch-Schönlein):current state of knowledge[J]. Curr Opin Rheumatol, 2013, 25(2):171-178.
Trnka P. Henoch-Schönlein purpura in children[J]. J Paediatr Child Health, 2013, 49(12):995-1003.
[4]
Rigante D, Castellazzi L, Bosco A, et al. Is there a crossroad between infections, genetics, and Henoch-Schönlein purpura[J]. Autoimmun Rev, 2013, 12(10):1016-1021.
[5]
Shin JI, Lee JS. Familial clusturing of Henoch-Schönlein purpura or IgA nephropathy:genetic background or environmental triggers[J]. Pediatr Dermatol, 2008, 25(6):651.
[6]
He X, Yu C, Zhao P, et al. The genetics of Henoch-Schönlein purpura:a systematic review and meta-analysis[J]. Rheumatol Int, 2013, 33(6):1387-1395.
[7]
Xie J, Liu Y, Wang L, et al. Expansion of circulating T follicular helper cells in children with acute Henoch-Schönlein purpura[J]. J Immunol Res, 2015, 2015:742535.
[8]
Johnson EF, Wetter DA, Lehman JS, et al. Leukocytoclastic vasculitis in children:clinical characteristics, subtypes, causes and direct immunofluorescence fndings of 56 biopsy-confrmed cases[J]. J Eur Acad Dermatol Venereol, 2016, 31(3):544-549.
Hu X, Tai J, Qu Z, et al. A lower proportion of regulatory B cells in patients with Henoch-Schönlein purpura nephritis[J]. PLoS One, 2016, 11(3):e0152368.
[12]
Kiryluk K, Moldoveanu Z, Sanders JT, et al. Aberrant glycosylation of IgA1 is inherited in both pediatric IgA nephropathy and Henoch-Schönlein purpura nephritis[J]. Kidney Int, 2011, 80(1):79-87.
Pan YX, Ye Q, Shao WX, et al. Relationship between immune parameters and organ involvement in children with HenochSchönlein purpura[J]. PLoS One, 2014, 9(12):e115261.
[15]
Kawasaki Y, Hosoya M, Suzuki H. Possible pathologenic role of interleukin-5 and eosino cationic protein in Henoch-Schönlein purpura nephritis[J]. Pediatr Int, 2005, 47(5):512-517.
Liu A, Zhang H. Detection of antiphospholipid antibody in children with Henoch-Schönlein purpura and central nervous system involvement[J]. Pediatr Neurol, 2012, 47(3):167-170.
[18]
Kawakami T, Takeuchi S, Soma Y. The presence of IgM antiphospholipid antibodies in patients with Henoch-Schönlein purpura and recurrent palpable purpura[J]. Arch Dermatol, 2011, 147(8):986-988.
[19]
Kimura S, Takeuchi S, Soma Y, et al. Raised serum levels of interleukins 6 and 8 and antiphospholipid antibodies in an adult patient with Henoch-Schönlein purpura[J]. Clin Exp Dermatol, 2013, 38(7):730-736.
[20]
Yu JH, Lee KB, Lee JE, et al. A case of elderly-onset crescentic Henoch-Schönlein purpura nephritis with hypocomplementemia and positive MPO-ANCA[J]. J Korean Med Sci, 2012, 27(8):957-960.
[21]
Chen T, Guo ZP, Li MM, et al. Tumour necrosis factor-like weak inducer of apoptosis (TWEAK), an important mediator of endothelial inflammation, is associated with the pathogenesis of Henoch-Schonlein purpura[J]. Clin Exp Immunol, 2011, 166(1):64-71.
[22]
Li YY, Li CR, Wang GB, et al. Investigation of the change in CD4+ T cell subset in children with Henoch-Schönlein purpura[J]. Rheumatol Int, 2012, 32(12):3785-3792.
[23]
Del Vecchio GC, Penza R, Altomare M, et al. Cytokine pattern and endothelium damage markers in Henoch-Schönlein purpura[J]. Immunopharmacol Immunotoxicol, 2008, 30(3):623-629.
[24]
Luo S, Liang G, Zhang P, et al. Aberrant histone modifcations in peripheral blood mononuclear cells from patients with HenochSchönlein purpura[J]. Clin Immunol, 2013, 146(3):165-175.
[25]
Chang H, Cao Y, Lin YI, et al. Association between toll-like receptor 6 expression and auxiliary T cells in the peripheral blood of pediatric patients with allergic purpura[J]. Exp Ther Med, 2015, 10(4):1536-1540.
[26]
Chang H, Zhang QY, Lin Y, et al. Correlation of TLR2 and TLR4 expressions in peripheral blood mononuclear cells to Th1- and Th2-type immune responses in children with HenochSchönlein purpura[J]. Int J Clin Exp Med, 2015, 8(8):13532-13539.
[27]
Kawasaki T, Kawai T. Toll-like receptor signaling pathways[J]. Front Immunol, 2014, 5:461.
[28]
Chen T, Guo ZP, Wang WJ, et al. Increased serum HMGB1 levels in patients with Henoch-Schönlein purpura[J]. Exp Dermatol, 2014, 23(6):419-423.
Yang YH, Huang YH, Lin YL, et al. Circulating IgA from acute stage of childhood Henoch-Schönlein purpura can enhance endothelial interleukin (IL)-8 production through MEK/ERK signalling pathway[J]. Clin Exp Immunol, 2006, 144(2):247-253.
[32]
Tabel Y, Mir S, Berdeli A. Interleukin 8 gene 2767 A/G polymorphism is associated with increased risk of nephritis in children with Henoch-Schönlein purpura[J]. Rheumatol Int, 2012, 32(4):941-947.
[33]
Xu H, Pan YX, Zhang J, et al. Lack of association between interleukin-8 gene +781 C/T polymorphism and HenochSchönlein purpura in childhood[J]. Iran J Allergy Asthma Immunol, 2016, 15(3):237-243.
[34]
Ding GX, Wang CH, Che RC, et al. Heat shock protein 70-2 and tumor necrosis factor-α gene polymorphisms in Chinese children with Henoch-Schönlein purpura[J]. World J Pediatr, 2016, 12(1):49-54.
[35]
Chen O, Zhu XB, Ren H, et al. The imbalance of Th17/Treg in Chinese children with Henoch-Schönlein purpura[J]. Int Immunopharmacol, 2013, 16(1):67-71.
[36]
Gülhan B, Orhan D, Kale G, et al. Studying cytokines of T helper cells in the kidney disease of IgA vasculitis (HenochSchönlein purpura)[J]. Pediatr Nephrol, 2015, 30(8):1269-1277.
[37]
Yang B, Tan X, Xiong X, et al. Effect of CD40/CD40L signaling on IL-10-producing regulatory B cells in Chinese children with Henoch-Schönlein purpura nephritis[J]. Immunol Res, 2016, doi:10.1007/s12026-016-8877-8.
[38]
Su Z, Lv X, Liu Y, et al. Circulating midkine in children with Henoch-Schönlein purpura:Clinical implications[J]. Int Immunopharmacol, 2016, 41:145.
[39]
Xu ED, Xiao YF, Wang JJ, et al. Association study between matrix metalloproteinase-9 gene (MMP9) polymorphisms and the risk of Henoch-Schönlein purpura in children[J]. Genet Mol Res, 2016, 15(2). doi:10.4238/gmr.15028095.
[40]
Mahajan N, Bisht D, Dhawan V, et al. Transcriptional expression and gelatinolytic activity of matrix metalloproteinases in Henoch-Schonlein purpura[J]. Acta Paediatr, 2010, 99(8):1248-1252.
[41]
Shin JI, Song KS, Kim H, et al. The gene expression profle of matrix metalloproteinases and their inhibitors in children with Henoch-Schönlein purpura[J]. Br J Dermatol, 2011, 164(6):1348-1355.
[42]
Erol M, Yigit O, Tasdemir M, et al. Potential of serum and urinary matrix metalloproteinase-9 levels for the early detection of renal involvement in children with Henoch-Schönlein purpura[J]. Iran J Pediatr, 2016, 26(4):e6129.
[43]
Ge W, Wang HL, Sun RP. Pentraxin 3 as a novel early biomarker for the prediction of Henoch-Schönlein purpura nephritis in children[J]. Eur J Pediatr, 2014, 173(2):213-218.
[44]
Yüksel S, Çağlar M, Evrengül H, et al. Could serum pentraxin 3 levels and IgM deposition in skin biopsies predict subsequent renal involvement in children with Henoch-Schönlein purpura[J]. Pediatr Nephrol, 2015, 30(6):969-974.
[45]
Yang YH, Tsai IJ, Chang CJ, et al. The interaction between circulating complement proteins and cutaneous microvascular endothelial cells in the development of childhood HenochSchönlein purpura[J]. PLoS One, 2015, 10(3):e0120411.
[46]
Roos A, Bouwman LH, van Gijlswijk-Janssen DJ, et al. Human IgA activates the complement system via the mannan-binding lectin pathway[J]. J Immunol, 2001, 167(5):2861-2868.
[47]
Hisano S, Matsushita M, Fujita T, et al. Activation of the lectin complement pathway in Henoch-Schönlein purpura nephritis[J]. Am J Kidney Dis, 2005, 45(2):295-302.
[48]
Constantinides MG, McDonald BD, Verhoef PA, et al. A committed precursor to innate lymphoid cells[J]. Nature, 2014, 508(7496):397-401.
[49]
He X, Yin W, Ding Y, et al. Higher serum angiotensinogen is an indicator of IgA vasculitis with nephritis revealed by comparative proteomes analysis[J]. PLoS One, 2015, 10(6):e0130536.
[50]
Cayci FS, Ekim M, Egin Y, et al. An analysis of the levels of the soluble form of the endothelial protein C receptor in children with Henoch-Schönlein purpura[J]. Pediatr Hematol Oncol, 2015, 32(2):115-122.
[51]
Li Y, Sui X, Zhu H, et al. Histopathological and immunological changes during the acute and recovery phase in HenochSchönlein purpura rabbit model[J]. Arch Dermatol Res, 2017, 309(1):21-30.
