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Biology subjects

Altman, E.

Publications and source records attributed to Altman, E..

3 recordsLinked to original sources

{Phi}X174 bacteriophage viability predicted by protein biophysical modeling

The relationship between genotype and phenotype underlies our ability to understand and predict evolution. Efforts to build genotype-phenotype (GP) maps have revealed several unifying rules: epistasis is pervasive, fitness effects are not normally distributed, and the GP map is non-linear and complicated for high-level phenotypes. A critical step in developing GP maps is evaluating how well predictive models do in explaining observed phenotypes. We utilize the simplicity of a bacteriophage ({Phi}X174) study system to test if an intermediate phenotype (predicted stability of the G capsid protein) explains more complex phenotypes. In doing so, we compare the predictive performance of free energies of folding and binding obtained using numerous molecular modeling methods as well as phylogenetic and basic biochemical/biophysical properties of amino acid substitutions. By creating a large mutational library, we find that {Phi}X174 tolerates about 50% of the amino acid substitutions we inserted into the G protein and that molecular modeling compliments other substitution models for predicting viability. Mutations predicted to have large destabilizing effects are especially informative and are almost universally detrimental. These large-effect substitutions often coincide with the most conserved residues in the G protein. Apart from large-effect mutations, our ability to predict {Phi}X174 phenotypes is fairly poor and we explore various potential confounding factors (e.g., codon bias) that could be considered to improve viability predictions.

molecular biology↗

Antigen-Specific modulation of MS/EAE by TCR-like Antibody Targeting Auto-Reactive Epitope

The development and application of human T-cell receptor (TCR)-like antibodies (TCRL) recognizing disease-specific peptide-MHC complexes may prove an important tool for basic research and therapeutic applications. Multiple Sclerosis is characterized by aberrant CD4 T cell response to self-antigens presented by class II MHC molecules. This led us to select a panel of TCRL Abs targeting the immunodominant autoantigenic epitope MOG35-55 derived from Myelin Oligodendrocyte Glycoprotein (MOG) presented on HLA-DR2 which is associated with Multiple Sclerosis (MS). We demonstrate that these TCRL Abs bind with high specificity to human HLA-DR2/ MOG35-55 derived MHC class II molecules and can detect APCs that naturally present the MS-associated autoantigen in humanized EAE transgenic mouse model. The TCRLs can block ex vivo and in vivo CD4 T-cell proliferation in response to MOG35-55 stimulation in an antigen-specific manner. Most significant, administration of TCRL to MOG35-55 induced EAE model in HLA-DR2 transgenic mice both prevents and regresses established EAE. TCRL function was associated with reduction of autoreactive pathogenic T cells infiltration into the CNS, along with modulation of activated CD11b+ macrophages/microglia APCs. Collectively, these findings demonstrate the combined action of TCRL Abs in blocking TCR-MHC interactions and modulating APC presentation and activation, leading to a profound antigen-specific inhibitory effect on the neuroinflammatory process, resulting in regression of EAE. Our study constitutes an in vivo proof-of-concept for the utility of TCR-like antibodies as antigen-specific immunomodulators for CD4-mediated autoimmune diseases such as multiple sclerosis (MS), validating the importance of the TCR-MHC axis as a therapeutic target for various autoimmune and inflammatory diseases.

immunology↗

Artificial Antigen Presenting Cells for Detection and Desensitisation of Auto-reactive T cells Associated with Type 1 Diabetes

Autoimmune diseases and in particular type 1 diabetes rely heavily on treatments that target the symptoms rather than prevent the underlying disease. One of the barriers to better therapeutic strategies is the inability to detect and efficiently target rare autoreactive T-cell populations that are major drivers of these conditions. Here, we develop a unique artificial antigen presenting cell (aAPC) system from biocompatible polymer particles that allows specific encapsulation of bioactive ingredients. Using our aAPC we demonstrate that we are able to detect rare autoreactive CD4 populations in human patients and using mouse models we demonstrate that our particles are able to induce desensitization in the autoreactive population. This system provides a promising tool that can be used in the prevention of autoimmunity before disease onset.

bioengineering↗