Immunological responsiveness of two lines of inbred mice, BALb/c and CBA, was studied by immunization of the animals with concentrated tick-borne encephalitis vaccine, and the role of cell-mediated immunity in formation of resistance of the two genetic lines of mice was evaluated. Determinations of the minimal immunizing dose of the vaccine revealed differences in parameters of the immunizing effect. Studies of the effect of TBE vaccine on the status of cell-mediated immunity by lymphocyte blastogenesis test led to a conclusion that vaccination of BALb/c mice contributed to the realization of the mitogenic effect of the antigen used to much greater extent.

Download full-text PDF

Source

Publication Analysis

Top Keywords

inbred mice
8
tick-borne encephalitis
8
cell-mediated immunity
8
[experimental study
4
study immunological
4
immunological reactivity
4
reactivity inbred
4
mice
4
mice varying
4
varying sensitivity
4

Similar Publications

Transcriptomic Profiling Reveals 17β-Estradiol Treatment Represses Ubiquitin-Proteasomal Mediators in Skeletal Muscle of Ovariectomized Mice.

J Cachexia Sarcopenia Muscle

February 2025

Division of Physical Therapy and Rehabilitation Science, Department of Family Medicine and Community Health, University of Minnesota, Minneapolis, Minnesota, USA.

Background: With a decline of 17β-estradiol (E2) at menopause, E2 has been implicated in the accompanied loss of skeletal muscle mass and strength. We aimed at characterizing transcriptomic responses of skeletal muscle to E2 in female mice, testing the hypothesis that genes and pathways related to contraction and maintenance of mass are differentially expressed in ovariectomized mice with and without E2 treatment.

Methods: Soleus and tibialis anterior (TA) muscles from C57BL/6 ovariectomized mice treated with placebo (OVX) or E2 (OVX + E2) for 60 days, or from skeletal muscle-specific ERα knockout (skmERαKO) mice and wild-type littermates (skmERαWT), were used for genome-wide expression profiling, quantitative real-time PCR and immunoblotting.

View Article and Find Full Text PDF

Abnormality of granulosa cells (GCs) is the critical cause of follicular atresia in premature ovarian failure (POF). RIPK3 is highly expressed in GCs derived from atretic follicles. We focus on uncovering how RIPK3 contributes to ovarian GC senescence.

View Article and Find Full Text PDF

Background: Asthma is a prevalent respiratory disease, and its management remains largely unsatisfactory. Mesenchymal stem cells (MSCs) have been demonstrated to be efficacious in reducing airway inflammation in experimental allergic diseases, representing a potential alternative treatment for asthma. Migrasomes are recently identified extracellular vesicles (EVs) generated in migrating cells and facilitate intercellular communication.

View Article and Find Full Text PDF

The incidence of obesity is increasing annually worldwide. A high-fat diet (HFD) causes intestinal barrier damage, but effective interventions are currently unavailable. Our previous work demonstrated the therapeutic effect of nobiletin on obese mice; thus, we hypothesized that nobiletin could reverse HFD-induced damage to the intestinal barrier.

View Article and Find Full Text PDF

Prophylactic and therapeutic effects of EsV3 on atherosclerotic lesions in ApoE mice.

BMC Cardiovasc Disord

January 2025

Department of Pharmacology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.

Background: Atherosclerosis (AS) is a major contributor to vascular disorders and represents a significant risk to human health. Currently, first-line pharmacotherapies are associated with substantial side effects, and the development of atherosclerosis is closely linked to dietary factors. This study evaluated the effects of a dietary supplement, EsV3, on AS in apolipoprotein E (ApoE) model mice.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!