中性粒细胞在炎症性皮肤病中的研究进展

doi:10.35541/cjd.20220865

Abstract

Abstract: 【Abstract】 Neutrophils are important in the immune defense system. Historically, neutrophils have been regarded as participants in innate immunity. Now, with the deepening of research, it has been found that neutrophils have regulatory properties, which can guide and regulate the local immune response by transmitting activation, inhibition and migration signals. In recent years, several studies related to inflammatory dermatoses have revealed the important roles of neutrophils in the occurrence and development of skin diseases. In psoriasis, neutrophils can indirectly enhance inflammatory response through interleukin-17/interleukin-23 axis or antimicrobial peptides; in systemic lupus erythematosus, neutrophils can regulate the interferon signal transduction and the formation of autoantibodies; in atopic dermatitis, neutrophils can affect bacterial colonization and itching, etc. In a word, the main mechanisms of action of neutrophils in inflammatory dermatoses include the involvement of neutrophils in immune cell communication networks to regulate disease development and the multiple roles of NETosis as a mode of neutrophil inflammatory death in disease immunity. This review summarizes the research progress on the roles of neutrophils in the occurrence and development of some inflammatory dermatoses.

Key words: Neutrophils, Psoriasis, Lupus erythematosus, systemic, Dermatitis, atopic, Dermatitis, contact, Neutrophilic dermatoses

Chen Xingyu, Yao Xu. Role of neutrophils in inflammatory dermatoses[J]. Chinese Journal of Dermatology,2024,e20220865. doi:10.35541/cjd.20220865

References ［68］

［1］	Burn GL, Foti A, Marsman G, et al. The neutrophil［J］. Immunity, 2021,54（7）:1377⁃1391. doi: 10.1016/j.immuni.2021.06.006.
［2］	Stark MA, Huo Y, Burcin TL, et al. Phagocytosis of apoptotic neutrophils regulates granulopoiesis via IL⁃23 and IL⁃17［J］. Immunity, 2005,22（3）:285⁃294. doi: 10.1016/j.immuni.2005.01. 011.
［3］	Nakabo S, Romo⁃Tena J, Kaplan MJ. Neutrophils as drivers of immune dysregulation in autoimmune diseases with skin manifestations［J］. J Invest Dermatol, 2022,142（3 Pt B）:823⁃833. doi: 10.1016/j.jid.2021.04.014.
［4］	Caielli S, Athale S, Domic B, et al. Oxidized mitochondrial nucleoids released by neutrophils drive type I interferon production in human lupus［J］. J Exp Med, 2016,213（5）:697⁃713. doi: 10.1084/jem.20151876.
［5］	Papayannopoulos V. Neutrophil extracellular traps in immunity and disease［J］. Nat Rev Immunol, 2018,18（2）:134⁃147. doi: 10.1038/nri.2017.105.
［6］	Eash KJ, Greenbaum AM, Gopalan PK, et al. CXCR2 and CXCR4 antagonistically regulate neutrophil trafficking from murine bone marrow［J］. J Clin Invest, 2010,120（7）:2423⁃2431. doi: 10.1172/JCI41649.
［7］	Pérez⁃Figueroa E, Álvarez⁃Carrasco P, Ortega E, et al. Neutrophils: many ways to die［J］. Front Immunol, 2021,12:631821. doi: 10.3389/fimmu.2021.631821.
［8］	Pires RH, Felix SB, Delcea M. The architecture of neutrophil extracellular traps investigated by atomic force microscopy［J］. Nanoscale, 2016,8（29）:14193⁃14202. doi: 10.1039/c6nr03416k.
［9］	Brinkmann V, Reichard U, Goosmann C, et al. Neutrophil extracellular traps kill bacteria［J］. Science, 2004,303（5663）:1532⁃1535. doi: 10.1126/science.1092385.
［10］	Garcia⁃Romo GS, Caielli S, Vega B, et al. Netting neutrophils are major inducers of type I IFN production in pediatric systemic lupus erythematosus［J］. Sci Transl Med, 2011,3（73）:73ra20. doi: 10.1126/scitranslmed.3001201.
［11］	Kienhöfer D, Hahn J, Stoof J, et al. Experimental lupus is aggravated in mouse strains with impaired induction of neutrophil extracellular traps［J］. JCI Insight, 2017,2（10）:e92920. doi: 10.1172/jci.insight.92920.
［12］	van der Linden M, van den Hoogen LL, Westerlaken G, et al. Neutrophil extracellular trap release is associated with antinuclear antibodies in systemic lupus erythematosus and anti⁃phospholipid syndrome［J］. Rheumatology （Oxford）, 2018,57（7）:1228⁃1234. doi: 10.1093/rheumatology/key067.
［13］	Carmona⁃Rivera C, Zhao W, Yalavarthi S, et al. Neutrophil extracellular traps induce endothelial dysfunction in systemic lupus erythematosus through the activation of matrix metalloproteinase⁃2［J］. Ann Rheum Dis, 2015,74（7）:1417⁃1424. doi: 10.1136/annrheumdis⁃2013⁃204837.
［14］	Radermecker C, Sabatel C, Vanwinge C, et al. Locally instructed CXCR4hi neutrophils trigger environment⁃driven allergic asthma through the release of neutrophil extracellular traps［J］. Nat Immunol, 2019,20（11）:1444⁃1455. doi: 10.1038/s41590⁃019⁃0496⁃9.
［15］	Guo Y, Kasahara S, Jhingran A, et al. During Aspergillus infection, monocyte⁃derived DCs, neutrophils, and plasmacytoid DCs enhance innate immune defense through CXCR3⁃dependent crosstalk［J］. Cell Host Microbe, 2020,28（1）:104⁃116.e4. doi: 10.1016/j.chom.2020.05.002.
［16］	Funch AB, Mraz V, Gadsbøll AØ, et al. CD8+ tissue⁃resident memory T cells recruit neutrophils that are essential for flare⁃ups in contact dermatitis［J］. Allergy, 2022,77（2）:513⁃524. doi: 10. 1111/all.14986.
［17］	Wang J, Wang J. Neutrophils, functions beyond host defense［J］. Cell Immunol, 2022,379:104579. doi: 10.1016/j.cellimm.2022. 104579.
［18］	Özcan A, Collado⁃Diaz V, Egholm C, et al. CCR7⁃guided neutrophil redirection to skin⁃draining lymph nodes regulates cutaneous inflammation and infection［J］. Sci Immunol, 2022,7（68）:eabi9126. doi: 10.1126/sciimmunol.abi9126.
［19］	Rodriguez⁃Rosales YA, Langereis JD, Gorris M, et al. Immunomodulatory aged neutrophils are augmented in blood and skin of psoriasis patients［J］. J Allergy Clin Immunol, 2021,148（4）:1030⁃1040. doi: 10.1016/j.jaci.2021.02.041.
［20］	Czerwińska J, Owczarczyk⁃Saczonek A. The role of the neutrophilic network in the pathogenesis of psoriasis［J］. Int J Mol Sci, 2022,23（3）:1840. doi: 10.3390/ijms23031840.
［21］	Dragan M, Sun P, Chen Z, et al. Epidermis⁃intrinsic transcription factor Ovol1 coordinately regulates barrier maintenance and neutrophil accumulation in psoriasis⁃like inflammation［J］. J Invest Dermatol, 2022,142（3 Pt A）:583⁃593.e5. doi: 10.1016/j.jid.2021.08.397.
［22］	Skrzeczynska⁃Moncznik J, Zabieglo K, Osiecka O, et al. Differences in staining for neutrophil elastase and its controlling inhibitor SLPI reveal heterogeneity among neutrophils in psoriasis［J］. J Invest Dermatol, 2020,140（7）:1371⁃1378.e3. doi: 10.1016/j.jid.2019.12.015.
［23］	Kim HJ, Roh JY, Jung Y. Eosinophils accelerate pathogenesis of psoriasis by supporting an inflammatory milieu that promotes neutrophil infiltration［J］. J Invest Dermatol, 2018,138（10）:2185⁃2194. doi: 10.1016/j.jid.2018.03.1509.
［24］	Metzemaekers M, Gouwy M, Proost P. Neutrophil chemoattractant receptors in health and disease: double⁃edged swords［J］. Cell Mol Immunol, 2020,17（5）:433⁃450. doi: 10.1038/s41423⁃020⁃0412⁃0.
［25］	Liu XT, Shi ZR, Lu SY, et al. Enhanced migratory ability of neutrophils toward epidermis contributes to the development of psoriasis via crosstalk with keratinocytes by releasing IL⁃17A［J］. Front Immunol, 2022,13:817040. doi: 10.3389/fimmu.2022. 817040.
［26］	Chen J, Zhu Z, Li Q, et al. Neutrophils enhance cutaneous vascular dilation and permeability to aggravate psoriasis by releasing matrix metallopeptidase 9［J］. J Invest Dermatol, 2021,141（4）:787⁃799. doi: 10.1016/j.jid.2020.07.028.
［27］	Chiang CC, Cheng WJ, Korinek M, et al. Neutrophils in psoriasis［J］. Front Immunol, 2019,10:2376. doi: 10.3389/fimmu.2019. 02376.
［28］	Lande R, Botti E, Jandus C, et al. The antimicrobial peptide LL37 is a T⁃cell autoantigen in psoriasis［J］. Nat Commun, 2014,5:5621. doi: 10.1038/ncomms6621.
［29］	Ganguly D, Chamilos G, Lande R, et al. Self⁃RNA⁃antimicrobial peptide complexes activate human dendritic cells through TLR7 and TLR8［J］. J Exp Med, 2009,206（9）:1983⁃1994. doi: 10. 1084/jem.20090480.
［30］	Xhindoli D, Pacor S, Benincasa M, et al. The human cathelicidin LL⁃37⁃⁃a pore⁃forming antibacterial peptide and host⁃cell modulator［J］. Biochim Biophys Acta, 2016,1858（3）:546⁃566. doi: 10.1016/j.bbamem.2015.11.003.
［31］	Herster F, Bittner Z, Archer NK, et al. Neutrophil extracellular trap⁃associated RNA and LL37 enable self⁃amplifying inflammation in psoriasis［J］. Nat Commun, 2020,11（1）:105. doi: 10.1038/s41467⁃019⁃13756⁃4.
［32］	Lambert S, Hambro CA, Johnston A, et al. Neutrophil extracellular traps induce human Th17 cells: effect of psoriasis⁃associated TRAF3IP2 genotype［J］. J Invest Dermatol, 2019,139（6）:1245⁃1253. doi: 10.1016/j.jid.2018.11.021.
［33］	Skrzeczynska⁃Moncznik J, Zabieglo K, Bossowski JP, et al. Eosinophils regulate interferon alpha production in plasmacytoid dendritic cells stimulated with components of neutrophil extracellular traps［J］. J Interferon Cytokine Res, 2017,37（3）:119⁃128. doi: 10.1089/jir.2016.0036.
［34］	Carmona⁃Rivera C, Kaplan MJ. Low⁃density granulocytes: a distinct class of neutrophils in systemic autoimmunity［J］. Semin Immunopathol, 2013,35（4）:455⁃463. doi: 10.1007/s00281⁃013⁃0375⁃7.
［35］	Fresneda Alarcon M, McLaren Z, Wright HL. Neutrophils in the pathogenesis of rheumatoid arthritis and systemic lupus erythematosus: same foe different M.O［J］. Front Immunol, 2021,12:649693. doi: 10.3389/fimmu.2021.649693.
［36］	Rahman S, Sagar D, Hanna RN, et al. Low⁃density granulocytes activate T cells and demonstrate a non⁃suppressive role in systemic lupus erythematosus［J］. Ann Rheum Dis, 2019,78（7）:957⁃966. doi: 10.1136/annrheumdis⁃2018⁃214620.
［37］	Mistry P, Nakabo S, O′Neil L, et al. Transcriptomic, epigenetic, and functional analyses implicate neutrophil diversity in the pathogenesis of systemic lupus erythematosus［J］. Proc Natl Acad Sci U S A, 2019,116（50）:25222⁃25228. doi: 10.1073/pnas.1908576116.
［38］	Kahlenberg JM, Carmona⁃Rivera C, Smith CK, et al. Neutrophil extracellular trap⁃associated protein activation of the NLRP3 inflammasome is enhanced in lupus macrophages［J］. J Immunol, 2013,190（3）:1217⁃1226. doi: 10.4049/jimmunol.1202388.
［39］	Bauernfeind FG, Horvath G, Stutz A, et al. Cutting edge: NF⁃kappaB activating pattern recognition and cytokine receptors license NLRP3 inflammasome activation by regulating NLRP3 expression［J］. J Immunol, 2009,183（2）:787⁃791. doi: 10.4049/jimmunol.0901363.
［40］	Gestermann N, Di Domizio J, Lande R, et al. Netting neutrophils activate autoreactive B cells in lupus［J］. J Immunol, 2018,200（10）:3364⁃3371. doi: 10.4049/jimmunol.1700778.
［41］	Lande R, Ganguly D, Facchinetti V, et al. Neutrophils activate plasmacytoid dendritic cells by releasing self⁃DNA⁃peptide complexes in systemic lupus erythematosus［J］. Sci Transl Med, 2011,3（73）:73ra19. doi: 10.1126/scitranslmed.3001180.
［42］	Diaz⁃Perez JA, Killeen ME, Yang Y, et al. Extracellular ATP and IL⁃23 form a local inflammatory circuit leading to the development of a neutrophil⁃dependent psoriasiform dermatitis［J］. J Invest Dermatol, 2018,138（12）:2595⁃2605. doi: 10.1016/j.jid.2018.05.018.
［43］	Toussaint M, Jackson DJ, Swieboda D, et al. Host DNA released by NETosis promotes rhinovirus⁃induced type⁃2 allergic asthma exacerbation［J］. Nat Med, 2017,23（6）:681⁃691. doi: 10.1038/nm.4332.
［44］	Inokuchi⁃Sakata S, Ishiuji Y, Katsuta M, et al. Role of eosinophil relative count and neutrophil⁃to⁃lymphocyte ratio in the assessment of severity of atopic dermatitis［J］. Acta Derm Venereol, 2021,101（7）:adv00491. doi: 10.2340/00015555⁃3838.
［45］	Impellizzieri D, Ridder F, Raeber ME, et al. IL⁃4 receptor engagement in human neutrophils impairs their migration and extracellular trap formation［J］. J Allergy Clin Immunol, 2019,144（1）:267⁃279.e4. doi: 10.1016/j.jaci.2019.01.042.
［46］	Heeb L, Egholm C, Boyman O. Evolution and function of interleukin⁃4 receptor signaling in adaptive immunity and neutrophils［J］. Genes Immun, 2020,21（3）:143⁃149. doi: 10. 1038/s41435⁃020⁃0095⁃7.
［47］	Woytschak J, Keller N, Krieg C, et al. Type 2 interleukin⁃4 receptor signaling in neutrophils antagonizes their expansion and migration during infection and inflammation［J］. Immunity, 2016,45（1）:172⁃184. doi: 10.1016/j.immuni.2016.06.025.
［48］	Egholm C, Özcan A, Breu D, et al. Type 2 immune predisposition results in accelerated neutrophil aging causing susceptibility to bacterial infection［J］. Sci Immunol, 2022,7（71）:eabi9733. doi: 10.1126/sciimmunol.abi9733.
［49］	Dhingra N, Suárez⁃Fariñas M, Fuentes⁃Duculan J, et al. Attenuated neutrophil axis in atopic dermatitis compared to psoriasis reflects TH17 pathway differences between these diseases［J］. J Allergy Clin Immunol, 2013,132（2）:498⁃501.e3. doi: 10.1016/j.jaci.2013.04.043.
［50］	Bitschar K, Staudenmaier L, Klink L, et al. Staphylococcus aureus skin colonization is enhanced by the interaction of neutrophil extracellular traps with keratinocytes［J］. J Invest Dermatol, 2020,140（5）:1054⁃1065.e4. doi: 10.1016/j.jid.2019. 10.017.
［51］	Geoghegan JA, Irvine AD, Foster TJ. Staphylococcus aureus and atopic dermatitis: a complex and evolving relationship［J］. Trends Microbiol, 2018,26（6）:484⁃497. doi: 10.1016/j.tim.2017.11.008.
［52］	Liew FY, Girard JP, Turnquist HR. Interleukin⁃33 in health and disease［J］. Nat Rev Immunol, 2016,16（11）:676⁃689. doi: 10. 1038/nri.2016.95.
［53］	Wang X, Li X, Chen L, et al. Interleukin⁃33 facilitates cutaneous defense against Staphylococcus aureus by promoting the develop⁃ment of neutrophil extracellular trap［J］. Int Immunopharmacol, 2020,81:106256. doi: 10.1016/j.intimp.2020.106256.
［54］	Walsh CM, Hill RZ, Schwendinger⁃Schreck J, et al. Neutrophils promote CXCR3⁃dependent itch in the development of atopic dermatitis［J］. Elife, 2019,8:e48448. doi: 10.7554/eLife.48448.
［55］	Strzepa A, Gurski CJ, Dittel LJ, et al. Neutrophil⁃derived myeloperoxidase facilitates both the induction and elicitation phases of contact hypersensitivity［J］. Front Immunol, 2020,11:608871. doi: 10.3389/fimmu.2020.608871.
［56］	Weber FC, Németh T, Csepregi JZ, et al. Neutrophils are required for both the sensitization and elicitation phase of contact hypersensitivity［J］. J Exp Med, 2015,212（1）:15⁃22. doi: 10.1084/jem.20130062.
［57］	Helou DG, Noël B, Gaudin F, et al. Cutting edge: Nrf2 regulates neutrophil recruitment and accumulation in skin during contact hypersensitivity［J］. J Immunol, 2019,202（8）:2189⁃2194. doi: 10.4049/jimmunol.1801065.
［58］	Shibuya R, Ishida Y, Hanakawa S, et al. CCL2⁃CCR2 signaling in the skin drives surfactant⁃induced irritant contact dermatitis through IL⁃1β⁃mediated neutrophil accumulation［J］. J Invest Dermatol, 2022,142（3 Pt A）:571⁃582.e9. doi: 10.1016/j.jid. 2021.07.182.
［59］	Saika A, Nagatake T, Kishino S, et al. 17（S）,18（R）⁃epoxyeicosatetraenoic acid generated by cytochrome P450 BM⁃3 from Bacillus megaterium inhibits the development of contact hypersensitivity via G⁃protein⁃coupled receptor 40⁃mediated neutrophil suppression［J］. FASEB Bioadv, 2020,2（1）:59⁃71. doi: 10.1096/fba.2019⁃00061.
［60］	Feldmeyer L, Ribero S, Gloor AD, et al. Neutrophilic dermatoses with unusual and atypical presentations［J］. Clin Dermatol, 2021,39（2）:261⁃270. doi: 10.1016/j.clindermatol.2020.10.012.
［61］	Filosa A, Filosa G. Neutrophilic dermatoses: a broad spectrum of disease［J］. G Ital Dermatol Venereol, 2018,153（2）:265⁃272. doi: 10.23736/S0392⁃0488.18.05841⁃8.
［62］	Weiss EH, Ko CJ, Leung TH, et al. Neutrophilic dermatoses: a clinical update［J］. Curr Dermatol Rep, 2022,11（2）:89⁃102. doi: 10.1007/s13671⁃022⁃00355⁃8.
［63］	Heath MS, Ortega⁃Loayza AG. Insights into the pathogenesis of Sweet′s syndrome［J］. Front Immunol, 2019,10:414. doi: 10. 3389/fimmu.2019.00414.
［64］	Nelson CA, Stephen S, Ashchyan HJ, et al. Neutrophilic dermatoses: pathogenesis, Sweet syndrome, neutrophilic eccrine hidradenitis, and Behçet disease［J］. J Am Acad Dermatol, 2018,79（6）:987⁃1006. doi: 10.1016/j.jaad.2017.11.064.
［65］	Maverakis E, Marzano AV, Le ST, et al. Pyoderma gangrenosum［J］. Nat Rev Dis Primers, 2020,6（1）:81. doi: 10.1038/s41572⁃020⁃0213⁃x.
［66］	Bonnekoh H, Scheffel J, Wu J, et al. Skin and systemic inflammation in Schnitzler′s syndrome are associated with neutrophil extracellular trap formation［J］. Front Immunol, 2019,10:546. doi: 10.3389/fimmu.2019.00546.
［67］	Eid E, Safi R, El Hasbani G, et al. Characterizing the presence of neutrophil extracellular traps in neutrophilic dermatoses［J］. Exp Dermatol, 2021,30（7）:988⁃994. doi: 10.1111/exd.14360.
［68］	Mistry P, Carmona⁃Rivera C, Ombrello AK, et al. Dysregulated neutrophil responses and neutrophil extracellular trap formation and degradation in PAPA syndrome［J］. Ann Rheum Dis, 2018,77（12）:1825⁃1833. doi: 10.1136/annrheumdis⁃2018⁃213746.

[1]	Wu Yubing, Wang Xiaoyu, An Binyi, Wu Yingying, Sang Hong, Kong Qingtao, . Role of cyclic guanosine monophosphate-adenosine monophosphate synthase-stimulator of interferon genes signaling pathway in the occurrence of psoriasis [J]. Chinese Journal of Dermatology, 2024, 0(3): 20230394-e20230394.
[2]	Zhu Tingting, Zhang Xuejun. Apremilast in the treatment of plaque psoriasis [J]. Chinese Journal of Dermatology, 2024, 0(3): 20230448-e20230448.
[3]	Hao Dan, Wang Yiyi, Xiao Yue, Yan Wei, Li Wei. Systemic treatment options for psoriasis in special areas [J]. Chinese Journal of Dermatology, 2024, 0(3): 20230190-e20230190.
[4]	Zong Yangyongyi, Ma Chujun, Su Zhonglan. Eczematization following the treatment of psoriasis with biological agents: pathogenesis and management [J]. Chinese Journal of Dermatology, 2024, 0(3): 20220578-e20220578.
[5]	Wang Yukun, Liu Jie. Application of deep learning in non-neoplastic dermatoses [J]. Chinese Journal of Dermatology, 2024, 0(3): 20220660-e20220660.
[6]	Wang Shiqi, Wang Aiping, Li Hang, Li Ruoyu. Comparison of dermoscopic features of toenail psoriasis and fingernail psoriasis [J]. Chinese Journal of Dermatology, 2024, 57(2): 161-165.
[7]	Fu Dandan, Li Jialin, Fu Xiuyu, Zhang Xinyu, Hu Hua, Song Xiangfeng, Tian Zhongwei. S100A10 protein expression in psoriatic lesions and its effect on psoriasis-like skin inflammation in mouse models [J]. Chinese Journal of Dermatology, 2023, 56(9): 839-844.
[8]	Liu Xiaoyang, Zhao Yan, Cai Lin, Zhang Jianzhong. Atopic dermatitis-like lesions appearing after interleukin-17 antagonist therapy in 4 cases of psoriasis: case analysis and literature review [J]. Chinese Journal of Dermatology, 2023, 56(9): 845-848.
[9]	Chen Xiaomin, Zhang Jingzhan, Ding Yuan, Kang Xiaojing. Metformin in the treatment of psoriasis [J]. Chinese Journal of Dermatology, 2023, 56(8): 799-802.
[10]	Tang Zhiming, Jing Mengqing, Lu Lu, Shan Xiao, Zhang Cuixia, Zhang Xiaoyu, Meng Sa. Effect of Xidi Liangxue recipe on the proliferation and apoptosis of HaCaT cells through the lncRNA NEAT1/miR-485-5p/STAT3 regulatory network [J]. Chinese Journal of Dermatology, 2023, 56(7): 642-650.
[11]	Committee on Psoriasis, Chinese Society of Dermatology. Guideline for the diagnosis and treatment of psoriasis in China （2023 edition） [J]. Chinese Journal of Dermatology, 2023, 56(7): 573-625.
[12]	Shan Ying, Chang Xiaotong, Zuo Yagang. Epitope spreading in autoimmune bullous diseases [J]. Chinese Journal of Dermatology, 2023, 56(7): 702-705.
[13]	Jiang Xiaoyan, Gao Min, Zhang Xiaoyan, Liu Ningyuan. Interleukin-17 and interleukin-23 inhibitors in the treatment of pustular psoriasis [J]. Chinese Journal of Dermatology, 2023, 56(7): 689-692.
[14]	China Dermatologist Association, Chinese Society of Dermatology, Xijing Hospital, Air Force Medical University, Chinese Dietary Guideline for Psoriasis Patients Task Force. Dietary guideline for patients with psoriasis in China （2023） [J]. Chinese Journal of Dermatology, 2023, 56(5): 389-401.
[15]	Jin Liping, Zhu Wu, Lu Yan, Liu Panpan, Tan Minjia, Wang Ying, Yang Jing, Xu Licong, Hu Kun, Kuang Yehong. Dietary intervention for the treatment of psoriasis [J]. Chinese Journal of Dermatology, 2023, 56(4): 357-360.

Role of neutrophils in inflammatory dermatoses

PDF

PDF (Mobile)

Knowledge

Abstract

Cite this article

share this article

References ［68］

Related Articles 15

Metrics

Comments

Recommended 10