دورية أكاديمية
أعرض في EDS

Preclinical stage abundance and nuclear antigen reactivity of faecal Immunoglobulin A vary among males and females of lupus-prone mouse models.

التفاصيل البيبلوغرافية
العنوان: Preclinical stage abundance and nuclear antigen reactivity of faecal Immunoglobulin A vary among males and females of lupus-prone mouse models.
المؤلفون: Gudi R; Department of Microbiology and Immunology, College of Medicine, Medical University of South Carolina, Charleston, South Carolina, USA., Roy S; Department of Microbiology and Immunology, College of Medicine, Medical University of South Carolina, Charleston, South Carolina, USA., Sun W; Department of Microbiology and Immunology, College of Medicine, Medical University of South Carolina, Charleston, South Carolina, USA., Vasu C; Department of Microbiology and Immunology, College of Medicine, Medical University of South Carolina, Charleston, South Carolina, USA.
المصدر: Immunology [Immunology] 2022 Apr; Vol. 165 (4), pp. 497-507. Date of Electronic Publication: 2022 Mar 01.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural
اللغة: English
بيانات الدورية: Publisher: Blackwell Scientific Publications Country of Publication: England NLM ID: 0374672 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1365-2567 (Electronic) Linking ISSN: 00192805 NLM ISO Abbreviation: Immunology Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Oxford : Blackwell Scientific Publications
مواضيع طبية MeSH: Immunoglobulin A* , Lupus Erythematosus, Systemic*, Animals ; Antigens, Nuclear ; Autoantibodies ; Disease Models, Animal ; Female ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Inbred MRL lpr
مستخلص: Systemic lupus erythematosus (SLE) is characterized by the production of pathogenic autoantibodies with nuclear antigen (nAg) specificity. Using (SWRxNZB)F1 (SNF1) mice, we showed higher levels of Immunoglobulin A (IgA) production in the intestine and the nAg reactivity of faecal IgA under lupus susceptibility. Here, we determined whether the faecal IgA abundance and nAg reactivity are higher in, different among, various lupus-prone preclinical models (MRL/lpr, NZBxNZW-F1, SNF1, NZM2410 and NZM2328). We also determined whether the faecal IgA nAg reactivity at preseropositive ages correlates with the eventual serum autoantibody levels in males and females of these mouse models. We show that age-dependent increase in the abundance and nAg reactivity of faecal IgA can vary among different lupus-prone mouse models. Importantly, faecal IgA in these mice show significant levels of nAg reactivity, starting as early as at juvenile age. Furthermore, the pre-seropositive stage nAg reactivity of faecal IgA in most lupus-prone strains correlates well with that of eventual, seropositive stage systemic autoantibody levels. Gender differences in serum autoantibody levels were preceded by similar differences in the faecal IgA abundance and nAg reactivity. These observations suggest that faecal IgA features, nAg reactivity particularly, could serve as a biomarker for early prediction of the eventual systemic autoimmunity in lupus-prone subjects.
(© 2022 John Wiley & Sons Ltd.)
References: Ann Rheum Dis. 1990 Jul;49(7):524-7. (PMID: 2383077)
Dis Markers. 2018 Sep 27;2018:4528547. (PMID: 30363714)
Immunity. 2014 Apr 17;40(4):608-20. (PMID: 24745335)
Clin Immunol. 2001 Sep;100(3):372-83. (PMID: 11513551)
J Immunol. 1999 Jul 1;163(1):359-66. (PMID: 10384136)
Trends Immunol. 2013 Apr;34(4):155-61. (PMID: 23083727)
Gut. 2003 Oct;52(10):1522-9. (PMID: 12970149)
Clin Exp Immunol. 2015 Jun;180(3):393-407. (PMID: 25603723)
J Invest Dermatol. 1991 Apr;96(4):478-83. (PMID: 1672542)
Adv Immunol. 2012;115:113-39. (PMID: 22608257)
J Exp Med. 2018 Aug 6;215(8):2019-2034. (PMID: 30042191)
Sci Rep. 2020 Aug 31;10(1):14258. (PMID: 32868790)
Science. 2010 Jun 25;328(5986):1705-9. (PMID: 20576892)
Nature. 2016 May 25;534(7606):263-6. (PMID: 27279225)
Cell Host Microbe. 2019 Jan 9;25(1):113-127.e6. (PMID: 30581114)
Int Immunol. 2017 Jun 1;29(6):263-276. (PMID: 28637300)
Sci Rep. 2016 Apr 05;6:24072. (PMID: 27044888)
Environ Health Perspect. 1999 Oct;107 Suppl 5:713-21. (PMID: 10502536)
Appl Environ Microbiol. 2018 Jan 31;84(4):. (PMID: 29196292)
PLoS One. 2013 Aug 12;8(8):e71458. (PMID: 23951169)
J Immunol. 1989 Mar 1;142(5):1482-6. (PMID: 2645362)
Lupus Sci Med. 2018 Jan 21;5(1):e000199. (PMID: 29387435)
Rheumatology (Oxford). 2020 Jan 1;59(1):90-98. (PMID: 31236574)
PLoS One. 2017 Nov 13;12(11):e0188037. (PMID: 29131864)
Rheumatology (Oxford). 2017 Apr 1;56(suppl_1):i88-i99. (PMID: 28013204)
Ann Rheum Dis. 2019 Jul;78(7):947-956. (PMID: 30782585)
Science. 2013 Mar 1;339(6123):1084-8. (PMID: 23328391)
Clin Immunol. 2013 Nov;149(2):211-8. (PMID: 23578823)
Sci Transl Med. 2018 May 2;10(439):. (PMID: 29720448)
Science. 2018 May 18;360(6390):795-800. (PMID: 29724905)
Clin Exp Immunol. 2015 Aug;181(2):323-37. (PMID: 25703185)
ScientificWorldJournal. 2014 Mar 05;2014:171028. (PMID: 24741342)
J Allergy Clin Immunol. 2017 Mar;139(3):1017-1025.e14. (PMID: 27531072)
Immunity. 2013 Aug 22;39(2):400-12. (PMID: 23973225)
Immunology. 2018 May;154(1):28-37. (PMID: 29338074)
J Autoimmun. 2020 Mar;108:102420. (PMID: 32019684)
Eur J Immunol. 1993 May;23(5):1146-52. (PMID: 8386666)
Cell Host Microbe. 2007 Nov 15;2(5):328-39. (PMID: 18005754)
J Exp Med. 1978 Nov 1;148(5):1198-215. (PMID: 309911)
Sci Transl Med. 2009 Nov 11;1(6):6ra14. (PMID: 20368178)
J Rheumatol. 1993 Jan;20(1):53-8. (PMID: 8441166)
Autoimmun Rev. 2010 Nov;10(1):3-7. (PMID: 20863908)
J Biol Chem. 2002 Aug 2;277(31):27622-8. (PMID: 12006568)
Semin Nephrol. 2007 Jan;27(1):12-21. (PMID: 17336685)
Arthritis Rheum. 1990 Feb;33(2):153-9. (PMID: 2407246)
Mucosal Immunol. 2016 Jul;9(4):907-16. (PMID: 26601902)
Lab Invest. 1993 Apr;68(4):419-26. (PMID: 8479150)
PLoS One. 2014 Sep 12;9(9):e106750. (PMID: 25215528)
Microbes Infect. 2001 Oct;3(12):1021-35. (PMID: 11580989)
Rheumatol Int. 1986;6(2):53-5. (PMID: 3764305)
Eur J Clin Microbiol Infect Dis. 2014 Sep;33(9):1467-75. (PMID: 24715155)
معلومات مُعتمدة: R01 AI138511 United States AI NIAID NIH HHS; R21 AI136339 United States AI NIAID NIH HHS
فهرسة مساهمة: Keywords: autoimmunity; biomarker; faecal IgA; faecal antibodies; lupus-prone mice; nuclear antigen; systemic lupus erythematosus (SLE)
المشرفين على المادة: 0 (Antigens, Nuclear)
0 (Autoantibodies)
0 (Immunoglobulin A)
تواريخ الأحداث: Date Created: 20220209 Date Completed: 20220425 Latest Revision: 20230402
رمز التحديث: 20230403
مُعرف محوري في PubMed: PMC9417274
DOI: 10.1111/imm.13459
PMID: 35138645
قاعدة البيانات: MEDLINE
الوصف
تدمد:1365-2567
DOI:10.1111/imm.13459