Evidence map›Paper›PMID 31620667›Full record

ArticleJournal of the Endocrine Society2019

Pathogenesis of Anti-PIT-1 Antibody Syndrome: PIT-1 Presentation by HLA Class I on Anterior Pituitary Cells.

Keitaro Kanie, Hironori Bando, Genzo Iguchi, Keiko Muguruma, Ryusaku Matsumoto, Ryoko Hidaka-Takeno, Yasuhiko Okimura, Masaaki Yamamoto, Yasunori Fujita, Hidenori Fukuoka and 5 more

Open access · goldAbstract read
In one paragraph

Article in Journal of the Endocrine Society, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.3field-weighted citation impact, top 19% of its field
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

13 citing papers in PubMed, 28 citations in OpenAlex.

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  10. Human pituitary development and application of iPSCs for pituitary disease.Cellular and molecular life sciences : CMLS · 2021
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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

15 authors at 4 institutions in 1 country.

Keitaro KanieDivision of Diabetes and Endocrinology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.ORCID 0000-0002-9004-9857
Hironori BandoDivision of Diabetes and Endocrinology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.
Genzo IguchiDivision of Diabetes and Endocrinology, Kobe University Hospital, Kobe, Japan.
Keiko MugurumaDepartment of iPS Cell Applied Medicine, Kansai Medical University, Hirakata, Japan.
Ryusaku MatsumotoDivision of Diabetes and Endocrinology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.
Ryoko Hidaka-TakenoDivision of Diabetes and Endocrinology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.
Yasuhiko OkimuraDepartment of Nutrition and Food Science, Kobe Women's University Graduate School of Life Sciences, Kobe, Japan.
Masaaki YamamotoDivision of Diabetes and Endocrinology, Kobe University Hospital, Kobe, Japan.
Yasunori FujitaDivision of Diabetes and Endocrinology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.
Hidenori FukuokaDivision of Diabetes and Endocrinology, Kobe University Hospital, Kobe, Japan.
Kenichi YoshidaDivision of Diabetes and Endocrinology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.
Kentaro SudaDivision of Diabetes and Endocrinology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.
Hitoshi NishizawaDivision of Diabetes and Endocrinology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.
Wataru OgawaDivision of Diabetes and Endocrinology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.
Yutaka TakahashiDivision of Diabetes and Endocrinology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.ORCID 0000-0002-1337-9246
Kobe University · JPKobe University Hospital · JPKansai Medical University · JPKobe Women's University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

contextAnti-pituitary-specific transcriptional factor-1 (anti-PIT-1) antibody syndrome is characterized by acquired and specific deficiencies in growth hormone, prolactin, and thyroid-stimulating hormone. Although PIT-1-reactive cytotoxic T lymphocytes (CTLs) have been speculated to recognize anterior pituitary cells and to cause the injury in the pathogenesis of the syndrome, it remains unclear whether endogenous PIT-1 protein is processed through the proteolytic pathway and presented as an antigen on anterior pituitary cells.

objectiveTo examine how PIT-1 protein is processed and whether its epitope is presented by major histocompatibility complex (MHC)/HLA class I on anterior pituitary cells. MATERIALS AND

methodsImmunofluorescence staining and proximity ligation assay (PLA) were performed using anti-PIT-1 antibody and patients' sera on PIT-1-expressing cell line GH3 cells and human induced pluripotent stem cell (iPSC)-derived pituitary tissues.

resultsPIT-1 was colocalized with MHC class I molecules, calnexin, and GM130 in the cytosol. PLA results showed that PIT-1 epitope was presented by MHC/HLA class I molecules on the cell surface of GH3 cells and iPSC-derived pituitary cells. The number of PIT-1/HLA complexes on the cell surface of pituitary cells in the patient was comparable with that in the control subject.

conclusionsOur data indicate that PIT-1 protein is processed in the antigen presentation pathway and that its epitopes are presented by in MHC/HLA class I on anterior pituitary cells, supporting the hypothesis that PIT-1-reactive CTLs caused the cell-specific damage. It is also suggested that number of epitope presentation was not associated with the pathogenesis of anti-PIT-1 antibody syndrome.

Indexed as

anti–PIT-1 antibody syndromecytotoxic T cellsHLA class Ihypophysitishypopituitarism

Identifiers

PMID31620667
PMCPMC6786005
OpenAlexW2970483791

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.