Paper · 6980965

Induction of neonatal tolerance to H-2k in B6 mice does not allow the emergence of T cells specific for H-2k plus vaccinia virus.

Schwartz DH and 1 other. J Exp Med, 1982. Cited by 5 papers, by iCite.

11 sourcespapers-2026-11-12-0.1.0

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ConductScience Library. Induction of neonatal tolerance to H-2k in B6 mice does not allow the emergence of T cells specific for H-2k plus vaccinia virus. Papers, record 6980965. Release papers-2026-11-12-0.1.0, 12 Nov 2026. https://conductscience.org/library/papers/6980965

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Paper

PubMed's record of the paper, with iCite's citation figures. No abstract is shown.

Title: Induction of neonatal tolerance to H-2k in B6 mice does not allow the emergence of T cells specific for H-2k plus vaccinia virus.; PubMed
Journal: J Exp Med; PubMed
Year: 1982; PubMed
Publication types: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.; PubMed
PubMed: https://pubmed.ncbi.nlm.nih.gov/6980965/; PubMed
DOI: https://doi.org/10.1084/jem.156.3.810; PubMed
PMC: https://pmc.ncbi.nlm.nih.gov/articles/PMC2186790/; PubMed
The journal: https://conductscience.org/library/journal-index/2985109R; PubMed
Citations, by iCite: 5; iCite
Relative citation ratio, by iCite: 0.11; iCite
Revised in PubMed: 2019-05-08; PubMed

Authors2

The authors in the order PubMed's record lists them, with the ORCID iDs it states.

Order	Author	Forename	Kind	ORCID iD
1	Schwartz DH	D H
2	Doherty PC	P C

Source PubMed

Topics15

NLM's MeSH indexing of the paper, its major topics first.

MeSH term	Major
Cytotoxicity, Immunologic	Major topic
H-2 Antigens	Major topic
Immune Tolerance	Major topic
T-Lymphocytes	Major topic
Vaccinia virus	Major topic
Animals
Antigens, Viral
Chimera
Female
Isoantigens
Male
Mice
Mice, Inbred C57BL
Mice, Inbred Strains
Models, Biological

Source PubMed

Grants3

Each grant PubMed's record writes, matched to the NIH project NIH's grant and paper links name for this paper, and each of those links the record does not write.

Grant, as the record writes it	Agency	Country	NIH project	Stated by	Source
AI-15412	NIAID NIH HHS	United States	R01AI015412	PubMed and NIH	NIH RePORTER
CA-10815	NCI NIH HHS	United States	P01CA010815	PubMed and NIH	NIH RePORTER
			P30CA010815	NIH	NIH RePORTER

Trials0

The trials whose ClinicalTrials.gov record lists the paper, and the trial numbers the paper's PubMed record names.

None in this release.

Comments and corrections0

PubMed's comments and corrections, NLM's own indexing: retractions first, then expressions of concern, errata and updates, and comments last.

None in this release.

References28

The papers the reference list in PubMed's record names, those in our copy of PubMed, in the list's order.

Order	PMID	Title	Journal	Year	In Papers	Source
1	4,576,586	Importance of chimerism in maintaining tolerance of skin allografts in mice.	J Immunol	1973	https://conductscience.org/library/papers/4576586	PubMed
2	4,275,043	An improved system for the assay of stimulation in mouse mixed leucocyte cultures.	J Immunol Methods	1974	https://conductscience.org/library/papers/4275043	PubMed
3	68,474	Nature of the antigenic complex recognized by T lymphocytes: specific sensitization by antigens associated with allogeneic macrophages.	Proc Natl Acad Sci U S A	1977	https://conductscience.org/library/papers/68474	PubMed
4	301,550	The generation of killer cells to trinitrophenyl-modified allogeneic targets by lymphocyte populations negatively selected to strong alloantigens.	J Exp Med	1977	https://conductscience.org/library/papers/301550	PubMed
5	305,460	The lymphoreticular system in triggering virus plus self-specific cytotoxic T cells: evidence for T help.	J Exp Med	1978	https://conductscience.org/library/papers/305460	PubMed
6	306,404	T cells specific for hapten-modified self are precommitted for self major histocompatibility complex antigens before encounter with the hapten.	J Exp Med	1978	https://conductscience.org/library/papers/306404	PubMed
7	307,186	Influence of the major histocompatibility complex on lymphocyte interactions in antibody formation.	Nature	1978	https://conductscience.org/library/papers/307186	PubMed
8	78,955	T-cell populations specifically depleted of alloreactive potential cannot be induced to lyse H-2-different virus-infected target cells.	J Exp Med	1978	https://conductscience.org/library/papers/78955	PubMed
9	80,023	Analysis of mechanisms of maintenance of neonatally induced tolerance to foreign alloantigens.	Scand J Immunol	1978	https://conductscience.org/library/papers/80023	PubMed
10	214,510	The biologic significance of alloreactivity. The ontogeny of T-cell sets specific for alloantigens or modified self antigens.	J Exp Med	1978	https://conductscience.org/library/papers/214510	PubMed

1 to 10 of 28

See all 28 references

Cited by2

The papers in our copy of PubMed whose reference list names this one, newest first. iCite, which reads more sources, counts 5 citations.

PMID	Title	Journal	Year	In Papers	Source
6,415,206	Cytotoxic T lymphocyte nonresponsiveness to the male antigen H-Y in the H-2Db mutants bm13 and bm14. Complementation of the response in F1 crosses with the I-Ab mutant bm12 nonresponder and failure of B6 or Db mutant mice tolerant of each other to respond to allogeneic male cells.	J Exp Med	1983	https://conductscience.org/library/papers/6415206	PubMed
6,232,678	Tolerance: facts and views--1983.	Surv Immunol Res	1984	https://conductscience.org/library/papers/6232678	PubMed

Genes0

The genes the Gene search release ties to the paper: Swiss-Prot's references first, then PubTator's text mining.

None in this release.

Drugs0

The drugs whose trials, in the Pipelines release, list the paper.

None in this release.

Data0

The data bank entries PubMed's record names. Trial numbers are under Trials.

None in this release.

Data dates

The date of each source this release read.

PubMed: 2026-11-06; PubMed
iCite: 2026-11-05; iCite
PMC's ID file: 2026-11-05; PMC's ID file
NIH RePORTER's grant and paper links: 2026-11-01; NIH RePORTER's grant and paper links
Trials: 2026-11-12
Gene search: 2026-11-11
Pipelines: 2026-09-18

Sources 11

ChEMBL, through Open TargetsCC BY-SA 3.0
ClinicalTrials.govNo license stated
HGNCCC0
iCiteCC BY 4.0
NCBI GenePublic domain (US government)
NIH RePORTER's grant and paper linksPublic domain
Open TargetsCC0 1.0
PMC's ID filePublic domain (US government)
PubMedNLM's terms
PubTator 3Public domain
UniProtCC BY 4.0

Each source's terms

ChEMBL, through Open TargetsCC BY-SA 3.0, for the parts from ChEMBL. Read on 8 Nov 2026 at https://platform-docs.opentargets.org/licence
ClinicalTrials.govnone stated
HGNCCC0: https://www.genenames.org/about/license/
iCiteCC BY 4.0
NCBI GeneNone named for the file. NCBI says information created by or for the US government on its site is in the public domain, and asks that NLM be acknowledged: https://www.ncbi.nlm.nih.gov/home/about/policies/
NIH RePORTER's grant and paper linksPublic domain (NIH RePORTER)
Open TargetsCC0 1.0. Open Targets asks that users cite its latest paper: Buniello et al. 2025, Open Targets Platform: facilitating therapeutic hypotheses building in drug discovery, Nucleic Acids Research 53(D1):D1467, PMID 39657122. Read on 8 Nov 2026 at https://platform-docs.opentargets.org/licence
PMC's ID fileNone named for the file. NCBI says information created by or for the US government on its site is in the public domain, and asks that NLM be acknowledged: https://www.ncbi.nlm.nih.gov/home/about/policies/
PubMedNLM's terms
PubTator 3Public domain
UniProtCC BY 4.0. UniProt's licence file: "All databases and documents in the UniProt FTP directory may be copied and redistributed freely, without advance permission, provided that this copyright statement is reproduced with each copy." UniProt asks that users cite its latest paper: The UniProt Consortium, UniProt: the Universal Protein Knowledgebase in 2025, Nucleic Acids Research 53:D609-D617, https://doi.org/10.1093/nar/gkae1010. Read on 9 Nov 2026 at https://www.uniprot.org/help/license

ClinicalTrials.gov's data carry an international copyright outside the United States: https://clinicaltrials.gov/about-site/terms-conditions.

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