Evidence map›Paper›PMID 26985768›Full record

ArticleOncotarget2016

CCR5 knockout suppresses experimental autoimmune encephalomyelitis in C57BL/6 mice.

Sun Mi Gu, Mi Hee Park, Hyung Mun Yun, Sang Bae Han, Ki Wan Oh, Dong Ju Son, Jae Suk Yun, Jin Tae Hong

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.5field-weighted citation impact, top 12% 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

28 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. Article
  3. The contributing role of CCR5 in dementia.Frontiers in neurology · 2025
    Review
  4. Review
  5. Article
  6. mScience China. Life sciences · 2023
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Calycosin-7-O-β-Glucoside Isolated fromInternational journal of molecular sciences · 2021
    Article
  19. Article
  20. Article
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

8 authors at 3 institutions in 1 country.

Sun Mi GuCollege of Pharmacy and Medical Research Center, Chungbuk National University, Cheongju-si, Chungcheongbuk-do, Republic of Korea.
Mi Hee ParkCollege of Pharmacy and Medical Research Center, Chungbuk National University, Cheongju-si, Chungcheongbuk-do, Republic of Korea.
Hyung Mun YunDepartment of Maxillofacial Tissue Regeneration, School of Dentistry and Research Center for Tooth and Periodontal Regeneration (MRC), Kyung Hee University, Seoul, Republic of Korea.
Sang Bae HanCollege of Pharmacy and Medical Research Center, Chungbuk National University, Cheongju-si, Chungcheongbuk-do, Republic of Korea.
Ki Wan OhCollege of Pharmacy and Medical Research Center, Chungbuk National University, Cheongju-si, Chungcheongbuk-do, Republic of Korea.
Dong Ju SonCollege of Pharmacy and Medical Research Center, Chungbuk National University, Cheongju-si, Chungcheongbuk-do, Republic of Korea.
Jae Suk YunPharmacological Research Division, National Institute of Food and Drug Safety Evaluation (NIFDS), Ministry of Food and Drug Safety (MFDS), Cheongju-si, Chungcheongbuk-do, Republic of Korea.
Jin Tae HongCollege of Pharmacy and Medical Research Center, Chungbuk National University, Cheongju-si, Chungcheongbuk-do, Republic of Korea.
Chungbuk National University · KRKyung Hee University · KRMinistry of Food and Drug Safety · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple sclerosis (MS) is an inflammatory disease in which myelin in the spinal cord is damaged. C-C chemokine receptor type 5 (CCR5) is implicated in immune cell migration and cytokine release in central nervous system (CNS). We investigated whether CCR5 plays a role in MS progression using a murine model, experimental autoimmune encephalomyelitis (EAE), in CCR5 deficient (CCR5-/-) mice. CCR5-/- and CCR5+/+ (wild-type) mice were immunized with myelin oligodendrocyte glycoprotein 35-55 (MOG35-55) followed by pertussis toxin, after which EAE paralysis was scored for 28 days. We found that clinical scoring and EAE neuropathology were lower in CCR5-/- mice than CCR5+/+ mice. Immune cells (CD3+, CD4+, CD8+, B cell, NK cell and macrophages) infiltration and astrocytes/microglial activation were attenuated in CCR5-/- mice. Moreover, levels of IL-1β, TNF-α, IFN-γ and MCP-1 cytokine levels were decreased in CCR5-/- mice spinal cord. Myelin basic protein (MBP) and CNPase were increased while NG2 and O4 were decreased in CCR5-/- mice, indicating that demyelination was suppressed by CCR5 gene deletion. These findings suggest that CCR5 is likely participating in demyelination in the spinal cord the MS development, and that it could serve as an effective therapeutic target for the treatment of MS.

Indexed as

AnimalsEncephalomyelitis, Autoimmune, ExperimentalHumansJurkat CellsMiceMice, Inbred C57BLMice, KnockoutReceptors, CCR5Spinal CordCCR5 protein, mouseReceptors, CCR5C-C chemokine receptor 5chemokinecytokineexperimental autoimmune encephalomyelitisImmune responseImmunityImmunology and Microbiology Sectionmultiple sclerosis

Identifiers

PMID26985768
PMCPMC4941248
OpenAlexW2320787276

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.