Evidence map›Paper›PMID 23175699›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2012

Molecular characterization of the early B cell response to pulmonary Cryptococcus neoformans infection.

Soma Rohatgi, Liise-anne Pirofski

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.3field-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

29 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Frontiers in cellular and infection microbiology · 2022
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Antibody immunity and natural resistance to cryptococcosis.Current tropical medicine reports · 2019
    Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Innate Immune Responses toJournal of fungi (Basel, Switzerland) · 2017
    Article
  20. Innate host defenses against Cryptococcus neoformans.Journal of microbiology (Seoul, Korea) · 2016
    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

2 authors at 1 institution in 1 country.

Soma RohatgiDivision of Infectious Diseases, Department of Medicine, Albert Einstein College of Medicine and Montefiore Medical Center, Bronx, NY 10461, USA.
Liise-anne Pirofski
Albert Einstein College of Medicine · US

Funding

WORD PROCESSORP30CA013330 · NCI · YESHIVA UNIVERSITY · PI THOMAS E ROHAN · 1985 to 2026
$111.2M
VARIABLE GENE DEFECTS AND PNEUMOCOCCAL SUSCEPTIBILITYR01AI044374 · NIAID · YESHIVA UNIVERSITY · PI PIROFSKI, LIISE-ANNE · 2001 to 2010
$2.7M
B cell subsets and immunity to cryptococcosisR01AI097096 · NIAID · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI PIROFSKI, LIISE-ANNE · 2012 to 2016
$2.7M
NCI NIH HHS P30 CA013330NCI NIH HHS P30CA013330NIAID NIH HHS R01 AI044374NIAID NIH HHS R01 AI097096
6 · The paper itself

Abstract

The role of B cells in host defense against fungi has been difficult to establish. We quantified and determined the molecular derivation of B-1a, B-1b, and B-2 B cell populations in C57BL/6 mice after pulmonary infection with Cryptococcus neoformans. Total B-1 and B-2 cell numbers increased in lungs and peritoneal cavity as early as day 1 postinfection, but lacked signs of clonal expansion. Labeled capsular (24067) and acapsular (Cap67) C. neoformans strains were used to identify C. neoformans-binding B cell subsets by flow cytometry. Peritoneal cavity B-1a B cells exhibited the most acapsular and capsular C. neoformans binding in C. neoformans-infected mice, and C. neoformans-selected B-1 B cells secreted laminarin- and C. neoformans-binding IgM. Single-cell PCR-based sequence analysis of B-1a, B-1b, and B-2 cell IgH V region H chain (V(H)) genes revealed increased usage of V(H)11 and V(H)12, respectively, in acapsular and capsular C. neoformans-selected B-1a cells. Germline V(H) segments were used, with capsular C. neoformans-selected cells having less junctional diversity than acapsular C. neoformans-selected cells. Further studies in B-1 B cell-depleted mice showed that these mice had higher brain and lung fungal burdens and less alveolar macrophage phagocytosis of C. neoformans than did control and B-1a B cell-reconstituted mice. Taken together, these results establish a mechanistic role for B-1 B cells in the innate B cell response to pulmonary infection with C. neoformans and reveal that IgM-producing B-1a cells, which express germline V(H) genes, bind C. neoformans and contribute to early fungal clearance. Thus, B-1a B cells provide a first line of defense during pulmonary C. neoformans infection in mice.

Indexed as

AnimalsB-Lymphocyte SubsetsCryptococcosisCryptococcus neoformansImmunoglobulin Heavy ChainsImmunoglobulin Variable RegionLung Diseases, FungalMiceMice, Inbred C57BLMolecular Sequence DataPeritoneal CavityImmunoglobulin Heavy ChainsImmunoglobulin Variable Region

Identifiers

PMID23175699
PMCPMC3518565
OpenAlexW2159305922

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.