TLR7, IFNγ, and T-bet: their roles in the development of ABCs in female-biased autoimmunity

Kira Rubtsova; Philippa Marrack; Anatoly V Rubtsov

doi:10.1016/j.cellimm.2014.12.002

TLR7, IFNγ, and T-bet: their roles in the development of ABCs in female-biased autoimmunity

Cell Immunol. 2015 Apr;294(2):80-3. doi: 10.1016/j.cellimm.2014.12.002. Epub 2014 Dec 13.

Authors

Kira Rubtsova¹, Philippa Marrack², Anatoly V Rubtsov³

Affiliations

¹ Howard Hughes Medical Institute, Denver, CO 80206, USA; Department of Biomedical Science, National Jewish Health and Department of Immunology and Microbiology, University of Colorado Health Sciences Center, Denver, CO 80206, USA. Electronic address: rubtsovak@njhealth.org.
² Howard Hughes Medical Institute, Denver, CO 80206, USA; Department of Biomedical Science, National Jewish Health and Department of Immunology and Microbiology, University of Colorado Health Sciences Center, Denver, CO 80206, USA; Department of Medicine, University of Colorado School of Medicine, Aurora, CO 80045, USA; Department of Biochemistry and Molecular Genetics, University of Colorado Health Sciences Center, Aurora, CO 80045, USA.
³ Howard Hughes Medical Institute, Denver, CO 80206, USA; Department of Biomedical Science, National Jewish Health and Department of Immunology and Microbiology, University of Colorado Health Sciences Center, Denver, CO 80206, USA.

Abstract

The majority of autoimmune diseases have a strong gender bias, affecting mostly females. Gender-specific factors like sex-hormones, the presence or absence of a second X chromosome, and gender-specific gut microbiota may contribute to this bias. In this review we will discuss the role of the X chromosome encoded toll-like receptor 7 (TLR7) and interferon gamma (IFNγ) in the development of autoimmunity. We will also review recent data indicating how these factors may affect an immune response in a gender-dependent manner.

Keywords: ABCs; Autoimmunity; Gender; IFNgamma; T-bet; TLR7.

Publication types

Research Support, N.I.H., Extramural
Review

MeSH terms

Animals
Autoimmune Diseases / genetics*
Autoimmune Diseases / immunology
B-Lymphocyte Subsets / immunology*
CD11c Antigen / biosynthesis
Female
Gene Dosage / immunology
Humans
Interferon-gamma / genetics*
Mice
Sex Characteristics
T-Box Domain Proteins / genetics*
Toll-Like Receptor 7 / genetics*

Substances

CD11c Antigen
T-Box Domain Proteins
T-box transcription factor TBX21
TLR7 protein, human
Toll-Like Receptor 7
Interferon-gamma

Abstract

Publication types

MeSH terms

Substances

Grants and funding