Student or educator? Sign up with your school email and get 6 months of Pro free.
Cited by 518

The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.

The Bare Lymphocyte Syndrome and the Regulation of MHC Expression

Open access
Reith, Walter, Mach, Bernard·2001·Annual Review of Immunology

Abstract

The bare lymphocyte syndrome (BLS) is a hereditary immunodeficiency resulting from the absence of major istocompatibility complex class II (MHCII) expression. Considering the central role of MHCII molecules in the development and activation of CD4+T cells, it is not surprising that the immune system of the patients is severely impaired. BLS is the prototype of a “disease of gene regulation.” The affected genes encode RFXANK, RFX5, RFXAP, and CIITA, four regulatory factors that are highly specific and essential for MHCII genes. The first three are subunits of RFX, a trimeric complex that binds to all MHCII promoters. CIITA is a non-DNA-binding coactivator that functions as the master control factor for MHCII expression. The study of RFX and CIITA has made major contributions to our comprehension of the molecular mechanisms controlling MHCII genes and has made this system into a textbook model for the regulation of gene expression.

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1146/annurev.immunol.19.1.331

Cites

4 of 4 references verified0 citation errors · 0 not checkable

Statistics

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Show all 4 references

Cited by

See all 518

Metadata

Authors
Reith, W., & Mach, B.
Venue
Annual Review of Immunology
Published
2001-04
Volume
19
Issue
1
Pages
331-373
ISSN
  • 0732-0582 (ISSN-L)
  • 1545-3278
OpenAlex
W1920211008
Cited by
518
References
4
FWCI
1.82
Type
journal article
Language
en
Open access
green

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review

How to cite

Cite CoChat for the checks on this page, and the paper for its own findings.

This page
CoChat. (2026). Citation check: The Bare Lymphocyte Syndrome and the Regulation of MHC Expression. https://app.cochat.ai/papers/10.1146/annurev.immunol.19.1.331
The paper
Reith, W., & Mach, B. (2001). The Bare Lymphocyte Syndrome and the Regulation of MHC Expression. Annual Review of Immunology. https://doi.org/10.1146/annurev.immunol.19.1.331

Data sources

Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.