Trogocytosis, an active cellular process involving the transfer of plasma membrane and attached cytosol during cell-to-cell contact, has been observed prominently in CD4 T cells interacting with antigen-presenting cells carrying antigen-loaded major histocompatibility complex (MHC) class II molecules. Despite the inherent absence of MHC class II molecules in CD4 T cells, they actively acquire these molecules from encountered antigen-presenting cells, leading to the formation of antigen-loaded MHC class II molecules-dressed CD4 T cells. Subsequently, these dressed CD4 T cells engage in antigen presentation to other CD4 T cells, revealing a dynamic mechanism of immune communication. The transferred membrane proteins through trogocytosis retain their surface localization, thereby altering cellular functions. Concurrently, the donor cells experience a loss of membrane proteins, resulting in functional changes due to the altered membrane properties. This chapter provides a focused exploration into trogocytosis-mediated transfer of immune regulatory molecules and its consequential impact on diverse immune responses.
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http://dx.doi.org/10.1007/978-3-031-62036-2_6 | DOI Listing |
ACS Nano
January 2025
Department of Bioengineering, University of Washington, Seattle, Washington 98195-5061, United States.
The recent development of modular universal chimeric antigen receptor (CAR) T-cell platforms that use bifunctional adaptor intermediates to redirect engineered T-cell effector function has greatly expanded the capabilities of adoptive T-cell therapy, enabling safer and more comprehensive cancer treatment. However, universal CAR receptor systems rely on unstable transient recognition of tag-coupled intermediates for T-cell activation, and the array of targeting intermediates has been limited to antibodies and small molecules. Addressing these shortcomings, we engineered universal CAR T-cell receptors that can be covalently modified with synthetic biomaterials by accelerated SpyCatcher003-SpyTag003 chemistry for cancer-cell targeting.
View Article and Find Full Text PDFPLoS Pathog
January 2025
Joint Research Center for Human Retrovirus Infection, Kumamoto University, Kumamoto, Japan.
We have demonstrated that the cellular protein M-Sec promotes the transmission of human T-cell leukemia virus type 1 (HTLV-1) in vitro and in vivo. Here, we show how HTLV-1 utilizes M-Sec for its efficient transmission. HTLV-1-infected CD4+ T cells expressed M-Sec at a higher level than uninfected CD4+ T cells.
View Article and Find Full Text PDFPLoS One
January 2025
Department of Microbiology, Mbarara University of Science and Technology, Uganda.
Background: Antiretroviral therapy (ART) restores cellular immunity, significantly reducing AIDS-related mortality and morbidity thus improving the quality of life among People living with HIV (PLHIV). Studies done in several countries show a decline in AIDS defining cancers (ADCs) with the introduction of ART however the increased longevity has led to the increase of Non-AIDS defining cancers (NADCs). The study was aimed at studying the changing spectrum and trends of cancer among Human Immunodeficiency Virus (HIV) patients in southwestern Uganda.
View Article and Find Full Text PDFJ Med Virol
February 2025
Infectious Diseases Department, University Hospital Montpellier & INSERM U1175, University Montpellier, Montpellier, France.
Despite viral suppression with antiretroviral therapy, immune nonresponders (INR) among people living with HIV (PLWH) still have a higher risk of developing AIDS-related and non-AIDS-related complications. Our study aimed to investigate the phenotype and functions of Natural Killer (NK) cells in INR, to better understand underlying mechanisms of immune nonresponse. Our cross-sectional study included PLWH aged over 45 with an undetectable HIV viral load sustained for at least 2 years.
View Article and Find Full Text PDFAllergy
January 2025
Department of Pediatrics and Adolescent Medicine, Juntendo University Graduate School of Medicine, Tokyo, Japan.
Background: IgE-mediated food allergy is accompanied by mucosal mast cell (MMC) hyperplasia in the intestinal mucosa. Intestinal MMC numbers correlate with the severity of food allergy symptoms. However, the mechanisms by which MMCs proliferate excessively are poorly understood.
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