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Elevated urinary IL-36γ in patients with active lupus nephritis and response to treatment.
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- Author(s): Majumder S;Majumder S; Singh P; Singh P; Chatterjee R; Chatterjee R; Pattnaik SS; Pattnaik SS; Aggarwal A; Aggarwal A
- Source:
Lupus [Lupus] 2021 May; Vol. 30 (6), pp. 921-925. Date of Electronic Publication: 2021 Feb 16.- Publication Type:
Journal Article- Language:
English - Source:
- Additional Information
- Source: Publisher: SAGE Publications Country of Publication: England NLM ID: 9204265 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1477-0962 (Electronic) Linking ISSN: 09612033 NLM ISO Abbreviation: Lupus Subsets: MEDLINE
- Publication Information: Publication: London : SAGE Publications
Original Publication: Houndmills, Basingstoke, Hampshire, UK : Scientific & Medical Division, Macmillan Press Ltd., c1991- - Subject Terms: Interleukin-1/*urine ; Lupus Erythematosus, Systemic/*immunology ; Lupus Nephritis/*immunology; Adolescent ; Adult ; Biomarkers/urine ; Case-Control Studies ; Enzyme-Linked Immunosorbent Assay ; Female ; Humans ; Interleukin-1/genetics ; Lupus Erythematosus, Systemic/urine ; Lupus Nephritis/urine ; Male ; Severity of Illness Index ; Young Adult
- Abstract: Introduction: IL-36 is a new member of the IL-1 family with pro-inflammatory properties. Serum levels of IL-36 are elevated in patients with Systemic Lupus Erythematosus (SLE). However, no data is available on urinary levels of IL-36 in Lupus Nephritis (LN). In psoriasis expression of IL-36 is site specific and expressed in skin. Hence, we studied urinary levels of IL-36 cytokines in SLE patients.
Methods: A total of 196 patients with SLE [97 active LN patients (ALN), 42 inactive LN (ILN) and 57 active lupus patients with no renal involvement (ANR)] and 25 healthy subjects were recruited for the study after obtaining informed consent. Urinary and plasma IL-36α, IL-36γ and IL-36Ra levels were measured by ELISA.
Results: Out of 196 patients 178 were females. Urinary IL-36γ levels in SLE patients [0(14.3) pg/ml] were significantly higher than healthy controls [0(0) pg/ml, (P < 0.01)]. Patients with ALN [0(40.6) pg/ml] had significantly higher IL-36γ when compared to ANR [0(0) pg/ml] as well as ILN [0(0) pg/ml]. Urinary IL-36γ levels in ALN patients had a fair correlation with renal SLEDAI (r = 0.26, P = 0.004).The levels reduced significantly post 3 months in patients with ALN. No inverse relationship was noted between IL-36Ra and IL-36α/IL36γ levels.
Conclusion: Urinary IL-36γ is produced locally in kidney, correlates with renal disease activity and reduces upon treatment, suggesting that it may have a role in pathogenesis of LN. - Contributed Indexing: Keywords: IL-36; SLE; cytokine; renal lupus; urine
- Accession Number: 0 (Biomarkers)
0 (IL36G protein, human)
0 (Interleukin-1) - Publication Date: Date Created: 20210217 Date Completed: 20211102 Latest Revision: 20211102
- Publication Date: 20240104
- Accession Number: 10.1177/0961203321995246
- Accession Number: 33593161
- Source:
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