ArticleImmunology2000
Recessive expression of the H2A-controlled immune response phenotype depends critically on antigen dose.
Article in Immunology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
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.
Who cites it
3 citing papers in PubMed, 3 citations in OpenAlex.
- Function and Potentials of M. tuberculosis Epitopes.Frontiers in immunology · 2014Review
- A novel human IgA monoclonal antibody protects against tuberculosis.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- H-2 alleles contribute to antigen 85-specific interferon-gamma responses during Mycobacterium tuberculosis infection.Cellular immunology · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Major histocompatibility complex (MHC) alleles acting as immune response genes are coexpressed in heterozygous individuals and therefore control of immune responses is usually codominant. As an exception to this rule, however, several examples of recessive immune responses have been ascribed to regulatory, e.g. suppressive, interactions. We report here that the recessive phenotype of both antibody and T-cell responses to the mycobacterial 16 000-MW antigen depends critically on a low antigen dose for immunization. On the basis of similar responses in hemi- and heterozygous mice, we suggest that the mechanism of recessive MHC control does not involve regulation by the low-responder allele. We also demonstrated mixed haplotype restriction of peptide recognition for a significant fraction of high-antigen-dose primed T cells. Their paucity under limiting antigen dose conditions may lead to the recessive expression of MHC control. In conclusion, our results suggest that recessive MHC control can be explained as a simple gene dosage effect under conditions where antigen is limiting, without a need for regulatory mechanisms.
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What OpenQuestion holds
Registered trials
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.