Evidence map›Paper›PMID 35196822›Full record

ArticleMicrobiology spectrum2022

CD84 is a Suppressor of T and B Cell Activation during Mycobacterium tuberculosis Pathogenesis.

Nan Zheng, Joy Fleming, Peilei Hu, Jianjian Jiao, Guoqin Zhang, Ruifang Yang, Chuanyou Li, Yi Liu, Lijun Bi, Hongtai Zhang

Open access · goldAbstract read
In one paragraph

Article in Microbiology spectrum, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

9 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Drug resistance mechanisms inFrontiers in pharmacology · 2026
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
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

10 authors at 3 institutions in 1 country.

Nan ZhengKey Laboratory of RNA Biology, Institute of Biophysics, Chinese Academy of Sciences, Beijing, China.
Joy FlemingKey Laboratory of RNA Biology, Institute of Biophysics, Chinese Academy of Sciences, Beijing, China.
Peilei HuHunan Chest Hospital, Changsha, Hunan Province, China.
Jianjian JiaoKey Laboratory of RNA Biology, Institute of Biophysics, Chinese Academy of Sciences, Beijing, China.
Guoqin ZhangKey Laboratory of RNA Biology, Institute of Biophysics, Chinese Academy of Sciences, Beijing, China.
Ruifang YangBeijing Chest Hospital, Capital Medical University, Beijing Tuberculosis and Thoracic Tumor Research Institute, Beijing Key Laboratory for Drug Resistant Tuberculosis Research, Beijing, China.
Chuanyou LiBeijing Chest Hospital, Capital Medical University, Beijing Tuberculosis and Thoracic Tumor Research Institute, Beijing Key Laboratory for Drug Resistant Tuberculosis Research, Beijing, China.
Yi LiuBeijing Chest Hospital, Capital Medical University, Beijing Tuberculosis and Thoracic Tumor Research Institute, Beijing Key Laboratory for Drug Resistant Tuberculosis Research, Beijing, China.
Lijun BiKey Laboratory of RNA Biology, Institute of Biophysics, Chinese Academy of Sciences, Beijing, China.
Hongtai ZhangKey Laboratory of RNA Biology, Institute of Biophysics, Chinese Academy of Sciences, Beijing, China.ORCID 0000-0001-9308-5872
Chinese Academy of Sciences · CNCapital Medical University · CNHunan Province Chest Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interest in host-directed therapies as alternatives/adjuncts to antibiotic treatment has resurged with the increasing prevalence of antibiotic-resistant tuberculosis (TB). Immunotherapies that reinvigorate immune responses by targeting immune checkpoints like PD-1/PD-L1 have proved successful in cancer therapy. Immune cell inhibitory receptors that trigger Mycobacterium tuberculosis-specific immunosuppression, however, are unknown. Here, we show that the levels of CD84, a SLAM family receptor, increase in T and B cells in lung tissues from M. tuberculosis-infected C57BL/6 mice and in peripheral blood mononuclear cells (PBMCs) from pulmonary TB patients. M. tuberculosis challenge experiments using CD84-deficient C57BL/6 mice suggest that CD84 expression likely leads to T and B cell immunosuppression during M. tuberculosis pathogenesis and also plays an inhibitory role in B cell activation. Importantly, CD84-deficient mice showed improved M. tuberculosis clearance and longer survival than M. tuberculosis-infected wild-type (WT) mice. That CD84 is a putative M. tuberculosis infection-specific inhibitory receptor suggests it may be a suitable target for the development of TB-specific checkpoint immunotherapies.

Indexed as

AnimalsB-LymphocytesFemaleHumansImmunosuppression TherapyLungLymphocyte ActivationMaleMiceMice, Inbred C57BLMice, KnockoutMycobacterium tuberculosisSignaling Lymphocytic Activation Molecule FamilyT-LymphocytesTuberculosis, PulmonaryCd84 protein, mouseSignaling Lymphocytic Activation Molecule FamilyCD84checkpoint immunotherapyMycobacterium tuberculosispathogenesis

Identifiers

PMID35196822
PMCPMC8865571
OpenAlexW4213443474

What OpenQuestion holds

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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.