Coxsackievirus B3 elicits a protective, sex-specific CD8 +T cell response in female mice

نویسندگان

چکیده

Abstract Sex is a significant contributor to the outcome of human infections. Males are frequently more susceptible viral, bacterial, and fungal infections, often attributed weaker immune responses. In contrast, heightened response in females enables better pathogen elimination but leaves predisposed autoimmune diseases. Unfortunately, underlying basis for sex-specific responses remains poorly understood. Here, we show sex difference CD8 +T cell an enteric virus, Coxsackievirus B3 (CVB3). We found that CVB3 induced expansion cells female Ifnar −/−mice not male −/−mice. Using recombinant virus expressing model epitope, viral-specific due bystander activation. also increased proportion number CD11a hiCD62L loCD8 mice, indicative T However, activation dampened by primary hormone, testosterone, mice. Finally, using antibodies deplete cells, required limit CVB3-induced disease These data demonstrate induces sex-dependent important viral clearance mice highlights importance differences pathogens. This work was funded K01 DK110216, R03 DK124749, Biomedical Research Grant from Indiana Clinical Translational Sciences Institute CMR.

برای دانلود باید عضویت طلایی داشته باشید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

HPV-E7 Delivered by Engineered Exosomes Elicits a Protective CD8+ T Cell-Mediated Immune Response

We developed an innovative strategy to induce a cytotoxic T cell (CTL) immune response against protein antigens of choice. It relies on the production of exosomes, i.e., nanovesicles spontaneously released by all cell types. We engineered the upload of huge amounts of protein antigens upon fusion with an anchoring protein (i.e., HIV-1 Nefmut), which is an inactive protein incorporating in exoso...

متن کامل

Coxsackievirus B3 protease 3C induces cell death in eukaryotic cells

Abstract: Coxsackievirus B3 (CVB3) is the most common agent known to cause viral myocarditis. The viral genome encodes a single polyprotein that is cleaved to produce several proteins by virally encoded proteases. Most of this proteolytic processing is catalyzed by a cysteine protease called 3C. The 3C protease plays major role in viral replication and cellular damage. To understand the mecha...

متن کامل

Coxsackievirus B3 infection reduces female mouse fertility

Previously we demonstrated coxsackievirus B3 (CVB3) infection during early gestation as a cause of pregnancy loss. Here, we investigated the impacts of CVB3 infection on female mouse fertility. Coxsackievirus-adenovirus receptor (CAR) expression and CVB3 replication in the ovary were evaluated by immunohistochemistry or reverse transcription-polymerase chain reaction (RT-PCR). CAR was highly ex...

متن کامل

Hormonal regulation of CD4(+) T-cell responses in coxsackievirus B3-induced myocarditis in mice.

Coxsackievirus B3 infection causes significant cardiac inflammation in male, but not female, B1.Tg.Ealpha mice. This gender difference in disease susceptibility correlates with selective induction of CD4(+) Th1 (gamma interferon-positive) cell responses in animals with testosterone, whereas estradiol promotes preferential CD4(+) Th2 (interleukin-4 positive [IL-4(+)]) cell responses. Differences...

متن کامل

Cardiac Fibroblasts Aggravate Viral Myocarditis: Cell Specific Coxsackievirus B3 Replication

Myocarditis is an inflammatory disease caused by viral infection. Different subpopulations of leukocytes enter the cardiac tissue and lead to severe cardiac inflammation associated with myocyte loss and remodeling. Here, we study possible cell sources for viral replication using three compartments of the heart: fibroblasts, cardiomyocytes, and macrophages. We infected C57BL/6j mice with Coxsack...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

ژورنال

عنوان ژورنال: Journal of Immunology

سال: 2023

ISSN: ['1550-6606', '0022-1767']

DOI: https://doi.org/10.4049/jimmunol.210.supp.59.37