Evidence map›Paper›PMID 31421081›Full record

ArticleJournal of immunological methods2019

Development of an anti-guinea pig CD4 monoclonal antibody for depletion of CD4+ T cells in vivo.

Brianne N Banasik, Clarice L Perry, Celeste A Keith, Nigel Bourne, Hubert Schäfer, Gregg N Milligan

Open access · greenAbstract read
In one paragraph

Article in Journal of immunological methods, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact, top 91% 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

4 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Model systems to studyFrontiers in cellular and infection microbiology · 2025
    Review
  3. Article
  4. 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

6 authors at 2 institutions in 2 countries.

Brianne N BanasikDepartment of Pediatrics, University of Texas Medical Branch, Galveston, TX, United States.
Clarice L PerryDepartment of Pediatrics, University of Texas Medical Branch, Galveston, TX, United States.
Celeste A KeithDepartment of Pediatrics, University of Texas Medical Branch, Galveston, TX, United States.
Nigel BourneDepartment of Pediatrics, University of Texas Medical Branch, Galveston, TX, United States; Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX, United States; Sealy Institute for Vaccine Sciences, University of Texas Medical Branch, Galveston, TX, United States.
Hubert SchäferMycotic and Parasitic Agents and Mycobacteria, Robert Koch-Institute, Nordufer 20, 13353 Berlin, Germany.
Gregg N MilliganDepartment of Pediatrics, University of Texas Medical Branch, Galveston, TX, United States; Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX, United States; Sealy Institute for Vaccine Sciences, University of Texas Medical Branch, Galveston, TX, United States. Electronic address: gnmillig@utmb.edu.
The University of Texas Medical Branch at Galveston · USRobert Koch Institute · DE

Funding

Induction, maintenance, and function of genital tract-resident CD8+ T cellsR01AI107784 · NIAID · UNIVERSITY OF TEXAS MED BR GALVESTON · PI MILLIGAN, GREGG N. · 2015 to 2019
$1.7M
NIAID NIH HHS R01 AI107784
6 · The paper itself

Abstract

The guinea pig serves as a useful animal model for a number of human diseases and has played an important role during development and testing of experimental vaccines and disease therapies. However, the availability of reagents to examine the immunological response in this species is very limited. Monoclonal antibodies (mAb) specific for cell surface proteins or products of immune cells have been useful tools for characterizing and quantifying immune responses in humans and in murine models of human disease, but very few similar reagents are available for characterizing and manipulating the immune response of guinea pigs. A rat IgG2a mAb specific for guinea pig CD4 has previously been described and was shown to inhibit T cell proliferation, but was inefficient at depleting CD4+ T cells in vivo. We hypothesized that the in vivo CD4+ T cell depletion function of this mAb could be improved by expression of the rat IgG2b heavy chain. We show that the purified mAb from an IgG2b class-switch variant, but not the parental IgG2a mAb, significantly depleted CD4+ T cells from secondary lymphoid tissue of guinea pigs. Further, treatment of guinea pigs with the IgG2b mAb at 2.0 mg/kg resulted in depletion of CD4+ T cells from peripheral blood and spleen. The use of this modified antibody to specifically alter the immune response of guinea pigs should prove useful in a number of guinea pig infectious disease models.

Indexed as

Antibody SpecificityAnimalsAntibodies, MonoclonalCD4-Positive T-LymphocytesFemaleGuinea PigsHybridomasImmunoglobulin Class SwitchingImmunoglobulin GLymphocyte DepletionRatsSpleenAntibodies, MonoclonalImmunoglobulin G

Identifiers

PMID31421081
PMCPMC6829055
OpenAlexW2967331968

What OpenQuestion holds

Textmetadata
LicenceTDM
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.