Evidence map›Paper›PMID 38459582›Full record

ArticleArthritis research & therapy2024

Low CD4 + T cell count is related to specific anti-nuclear antibodies, IFNα protein positivity and disease activity in systemic lupus erythematosus pregnancy.

Agnes Torell, Marit Stockfelt, Kaj Blennow, Henrik Zetterberg, Tansim Akhter, Dag Leonard, Lars Rönnblom, Sofia Pihl, Muna Saleh, Christopher Sjöwall and 12 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Arthritis research & therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

22 authors.

Agnes TorellDepartment of Rheumatology and Inflammation Research, Institute of Medicine, Sahlgrenska Academy at the University of Gothenburg, Guldhedsgatan 10A, 405 30, Gothenburg, Sweden. agnes.torell.bjorkman@gu.se.
Marit StockfeltDepartment of Rheumatology and Inflammation Research, Institute of Medicine, Sahlgrenska Academy at the University of Gothenburg, Guldhedsgatan 10A, 405 30, Gothenburg, Sweden.
Kaj BlennowDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Henrik ZetterbergDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Tansim AkhterDepartment of Women's and Children's Health, Section of Obstetrics and Gynecology, Uppsala University, Uppsala, Sweden.
Dag LeonardDepartment of Medical Sciences, Rheumatology, Uppsala University, Uppsala, Sweden.
Lars RönnblomDepartment of Medical Sciences, Rheumatology, Uppsala University, Uppsala, Sweden.
Sofia PihlDepartment of Obstetrics and Gynecology, Linköping University Hospital, Linköping, Sweden.
Muna SalehDivision of Inflammation and Infection, Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden.
Christopher SjöwallDivision of Inflammation and Infection, Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden.
Helena StrevensDepartment of Obstetrics and Gynecology, Institute of Clinical Sciences, Skåne University Hospital, Lund, Sweden.
Andreas JönsenDepartment of Clinical Sciences Lund, Rheumatology, Lund University, Skåne University Hospital, Lund, Sweden.
Anders A BengtssonDepartment of Clinical Sciences Lund, Rheumatology, Lund University, Skåne University Hospital, Lund, Sweden.
Estelle TrysbergRheumatology, Sahlgrenska University Hospital, Gothenburg, Sweden.
Maria Majczuk SennströmDepartment of Womens and Childrens Health, Division for Obstetrics and Gynecology, Karolinska University Hospital, Karolinska Institute, Stockholm, Sweden.
Agneta ZickertDivision of Rheumatology, Department of Medicine Solna, Karolinska Institute, Karolinska University Hospital, Stockholm, Sweden.
Elisabet SvenungssonDivision of Rheumatology, Department of Medicine Solna, Karolinska Institute, Karolinska University Hospital, Stockholm, Sweden.
Iva GunnarssonDivision of Rheumatology, Department of Medicine Solna, Karolinska Institute, Karolinska University Hospital, Stockholm, Sweden.
Johan BylundDepartment of Oral Microbiology and Immunology, Institute of Odontology, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden.
Bo JacobssonDepartment of Obstetrics and Gynecology, Sahlgrenska University Hospital, Gothenburg, Sweden.
Anna RudinDepartment of Rheumatology and Inflammation Research, Institute of Medicine, Sahlgrenska Academy at the University of Gothenburg, Guldhedsgatan 10A, 405 30, Gothenburg, Sweden.
Anna-Carin LundellDepartment of Rheumatology and Inflammation Research, Institute of Medicine, Sahlgrenska Academy at the University of Gothenburg, Guldhedsgatan 10A, 405 30, Gothenburg, Sweden.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLymphopenia, autoantibodies and activation of the type I interferon (IFN) system are common features in systemic lupus erythematosus (SLE). We speculate whether lymphocyte subset counts are affected by pregnancy and if they relate to autoantibody profiles and/or IFNα protein in SLE pregnancy.

methodsRepeated blood samples were collected during pregnancy from 80 women with SLE and 51 healthy controls (HC). Late postpartum samples were obtained from 19 of the women with SLE. Counts of CD4 + and CD8 + T cells, B cells and NK cells were measured by flow cytometry. Positivity for anti-nuclear antibodies (ANA) fine specificities (double-stranded DNA [dsDNA], Smith [Sm], ribonucleoprotein [RNP], chromatin, Sjögren's syndrome antigen A [SSA] and B [SSB]) and anti-phospholipid antibodies (cardiolipin [CL] and β

resultsWomen with SLE had lower counts of all lymphocyte subsets compared to HC throughout pregnancy, but counts did not differ during pregnancy compared to postpartum. Principal component analysis revealed that low lymphocyte subset counts differentially related to autoantibody profiles, cluster one (anti-dsDNA/anti-Sm/anti-RNP/anti-Sm/RNP/anti-chromatin), cluster two (anti-SSA/anti-SSB) and cluster three (anti-CL/anti-β2GPI), IFNα protein levels and disease activity. CD4 + T cell counts were lower in women positive to all ANA fine specificities in cluster one compared to those who were negative, and B cell numbers were lower in women positive for anti-dsDNA and anti-Sm compared to negative women. Moreover, CD4 + T cell and B cell counts were lower in women with moderate/high compared to no/low disease activity, and CD4 + T cell count was lower in IFNα protein positive relative to negative women. Finally, CD4 + T cell count was unrelated to treatment.

conclusionLymphocyte subset counts are lower in SLE compared to healthy pregnancies, which seems to be a feature of the disease per se and not affected by pregnancy. Our results also indicate that low lymphocyte subset counts relate differentially to autoantibody profiles, IFNα protein levels and disease activity, which could be due to divergent disease pathways.

Indexed as

Lupus Erythematosus, SystemicLymphopeniaT-Lymphocytopenia, Idiopathic CD4-PositiveAntibodies, AntinuclearAutoantibodiesDNAFemaleHumansInterferon-alphaPregnancyAntibodies, AntinuclearAutoantibodiesDNAInterferon-alphaAutoantibodiesInterferon alphaLymphocyte countPregnancySystemic lupus erythematosus (SLE)

Identifiers

PMID38459582
PMCPMC10924387

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