Dr. Michael Opata

RECAPP 2019 and RECAPP 2020 Award Winner. Education: Ph.D. University of Kentucky College of Medicine, Lexington, KY; M.S. Jackson State University, Jackson, MS; B.S. Rust College, Holly Spring, MS. Professional Experience: Assistant Professor, Appalachian State University, Department of Biology; Postdoctoral Fellow, University of Texas Medical Branch, Division of Infectious Diseases; Graduate Researcher, University of Kentucky, Department of Microbiology, Immunology and Molecular Genetics. Teaching Specialties: Immunology and Human Microbiology. Areas of Research Interest: Immunoparasitology, Cellular and Molecular Immunology, Infectious Diseases, Flow Cytometry, Effects of malnutrition on infectious diseases, and Childhood malaria.

There are 8 included publications by Dr. Michael Opata :

TitleDateViewsBrief Description
Aqueous Vernomia amygdalina Extracts Alter MCF-7 Cell Membrane Permeability And Efflux 2006 380 Breast cancer is the second leading cause of cancer related deaths of women in the United States. Several treatment strategies have been developed over the past decade to reduce cancer morbidity and mortality rates. While mortality rates have decline...
B Cell Production Of Tumor Necrosis Factor In Response To Pneumocystis murina Infection In Mice 2013 387 Pneumocystis species are opportunistic fungal pathogens that induce tumor necrosis factor (TNF) production by alveolar macrophages. Here we report that B cells from the draining lymph nodes as well as lung CD4(+) T cells are important producers of TN...
B Lymphocytes Are Required During The Early Priming Of CD4 T Cells For Clearance Of Pneumocystis Infection In Mice 2015 411 B cells play a critical role in the clearance of Pneumocystis. In addition to production of Pneumocystis-specific Abs, B cells are required during the priming phase for CD4+ T cells to expand normally and generate memory. Clearance of Pneumocystis wa...
Chronic Plasmodium chabaudi Infection Generates CD4 Memory T Cells With Increased T Cell Receptor Sensitivity But Poor Secondary Expansion And Increased Apoptosis 2016 415 Exposure to blood-stage malaria infection is often persistent, leading to generation of CD4 effector and effector memory T cells that contribute to protection. We showed previously that chronic exposure to blood-stage Plasmodium chabaudi offers the b...
Early Effector Cells Survive The Contraction Phase In Malaria Infection And Generate Both Central And Effector Memory T Cells 2015 466 CD4 T cells orchestrate immunity against blood-stage malaria. However, a major challenge in designing vaccines to the disease is poor understanding of the requirements for the generation of protective memory T cells (Tmem) from responding effector T ...
Gamma Delta And Natural Killer Cells In Splenocytes Of Young Mice Protect Immunocompromised Mice From Death In Plasmodium Chabaudi Infection (ABSTRACT ONLY: Poster) 2020 101 Immunity to malaria requires an elongated time to develop. While there has been advancement in understanding of the immune response to malaria, knowledge on immunity of the disease in children under five is limited due to the lack of a reliable young...
IFN-y And IL-21 Double Producing T Cells Are Bcl6-Independent And Survive Into The Memory Phase In Plasmodium chabaudi Infection 2015 31 CD4 T cells are required to fight malaria infection by promoting both phagocytic activity and B cell responses for parasite clearance. In Plasmodium chabaudi infection, one specific CD4 T cell subset generates anti-parasitic IFN-y and the antibody-pr...
Protection By And Maintenance Of CD4 Effector Memory And Effector T Cell Subsets In Persistent Malaria Infection 2018 418 Protection at the peak of Plasmodium chabaudi blood-stage malaria infection is provided by CD4 T cells. We have shown that an increase in Th1 cells also correlates with protection during the persistent phase of malaria; however, it is unclear how the...