DiLorenzo, T. | Search bioRxiv

bioRxiv2024

TrAQ: a novel, versatile, semi-automated, two-dimensional motor behavioural tracking software

We present TrAQ, a new MATLAB-based two-dimensional tracking software for Open Field video analysis of unmarked single animal, featuring minimum user intervention. We developed TrAQ with the purpose to automatically count the in-plane rotations, an important parameter in the 6-hydroxydopamine hemiparkinsonian rat model and in many rodent models of neurodegenerative diseases, a very time-consuming manual task for highly trained human operators. In addition, TrAQ allows automatic recognition of the animal within a user defined arena providing a quantitative measurement of the body centroid and the two extremities positions. A full range of quantitative kinematic behavioral parameters are automatically calculated, and the optional shape erosion feature adds usage flexibility. TrAQ, free and non-species-specific application, was quantitively tested with rodents and on a qualitative basis with zebrafish, and invertebrate animal models. Quantitative results were successfully validated against a commercial software (for tracking) and manual annotation (for rotations in an hemiparkinsonian rat model). This is a widely used model in preclinical research to study postural instability and motor asymmetry. TrAQ allows the characterization of motor asymmetry using non-invasive tools, thus appreciating the spontaneous Open Field behaviour of unmarked single animal, with minimum user intervention.

animal behavior and cognition↗

bioRxiv2018

HLA-B*39:06 Efficiently Mediates Type 1 Diabetes in a Mouse Model Incorporating Reduced Thymic Insulin Expression

Type 1 diabetes (T1D) is characterized by T cell-mediated destruction of the insulin-producing {beta}cells of the pancreatic islets. Among the loci associated with T1D risk, those most predisposing are found in the MHC region. HLA-B*39:06 is the most predisposing class I MHC allele and is associated with an early age of onset. To establish an NOD mouse model for the study of HLA-B*39:06, we expressed it in the absence of murine class I MHC. HLA-B*39:06 was able to mediate the development of CD8 T cells, support lymphocytic infiltration of the islets, and confer T1D susceptibility. Because reduced thymic insulin expression is associated with increased T1D risk in patients, we incorporated this in our model as well, finding that HLA-B*39:06-transgenic NOD mice with reduced thymic insulin expression have an earlier age of disease onset and a higher overall prevalence as compared to littermates with typical thymic insulin expression. This was despite virtually indistinguishable blood insulin levels, T cell subset percentages, and TCR V{beta} family usage, indicating that reduced thymic insulin expression does not impact T cell development on a global scale. Rather, we propose that it allows the thymic escape of insulin-reactive HLA-B*39:06-restricted T cells which participate in {beta} cell destruction. We also found that in mice expressing either HLA-B*39:06 or HLA-A*02:01 in the absence of murine class I MHC, HLA transgene identity alters TCR V{beta} usage, which may contribute to varying diabetogenic CD8 T cell repertoires in the presence of different HLA class I alleles.

immunology↗