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Host Defense and Parasite Evasion
Published in Eric S. Loker, Bruce V. Hofkin, Parasitology, 2023
Eric S. Loker, Bruce V. Hofkin
Data for Trichomonas vaginalis are similarly ambiguous. A comparison of asymptomatic and symptomatic mice infected with this parasite found that the inflammatory Th-1-type cytokines were actually elevated in asymptomatic animals. Inflammation, however, is believed to be an important factor in the pathology associated with trichomoniasis. Furthermore, neutrophils are known to be important players in an immune response to T. vaginalis, and it has recently been demonstrated that these leukocytes kill T. vaginalis utilizing trogocytosis (Figure 4.17) as opposed to phagocytosis. In this process, neutrophils first swarm around the parasite, and then, utilizing serine proteases, take repeated small “bites,” ultimately resulting in the death of the trogocytosed protozoan. This process is remarkably similar to that used by Entamoeba histolytica, to ingest portions of host cells, suggesting that trogocytosis evolved very early in eukaryotic evolution, and that it may be more common than previously believed. Trogocytosis requires physical contact between neutrophils and T. vaginalis, and it appears that antibody, specifically IgG, frequently acts as an opsonin, facilitating this contact. Such data nicely illustrates the interplay between adaptive and innate immunity. Interestingly, it also suggests that the cysteine proteases released by T. vaginalis represent a form of immune evasion in which they degrade IgG, and thus interfere with the ability of the antibody to facilitate trogocytosis.
Trogocytosis and fratricide killing impede MSLN-directed CAR T cell functionality
Published in OncoImmunology, 2022
Esther Schoutrop, Stefanie Renken, Isabella Micallef Nilsson, Paula Hahn, Thomas Poiret, Rolf Kiessling, Stina L Wickström, Jonas Mattsson, Isabelle Magalhaes
In B cell malignancies, the loss or downregulation of surface antigen on tumor cells has been demonstrated to be a major mechanism of resistance against successful CD19-CAR T cell therapy.13 Recently, CAR T cell mediated trogocytosis has been reported to contribute to tumor antigen escape and CAR T cell dysfunction. Trogocytosis is an active process occurring at the immunological synapse, where membrane and membrane-associated molecules are transferred from antigen-presenting or target cells to effector cells.14–16 Trogocytosis-mediated loss of surface antigen poses yet another challenge to successful CAR T cell therapy of solid tumors expressing MSLN, as MSLN expression is naturally heterogeneous and trogocytosis may further lower expression. The induction of CAR-independent tumor cell lysis, referred to as ‘bystander killing’, could alleviate the lack of universal tumor antigen expression.17,18 To successfully translate CAR T cell therapy to solid tumors, elucidating the mechanisms affecting CAR T cell functionality in vitro is fundamental.
Expression of HLA-G and KIR2DL4 receptor in chorionic villous in missed abortion
Published in Gynecological Endocrinology, 2020
Olesya Bespalova, Margarita Bakleicheva, Tatiana Ivashchenko, Tatiana Tral, Gulrukhsor Tolibova, Igor Kogan
HLA-G expression is not strictly associated with the protection of embryo/fetus against the attack of maternal cells, but it is engaged with tissue remodeling. Expressed or secreted HLA-G molecules by extravillous trophoblast cells (EVT) regulate their decidual and endovascular invasion [5,6]. In the transplantation setting, the induction of HLA-G expression correlates with increased transplant acceptance. In healthy individuals, the best-documented evidence of HLA-G protein expression occurs on fetal trophoblast cells that invade the maternal decidua during early pregnancy. EVT cells progressively replace endothelial cells on the walls of uterine spiral arteries, increasing their diameter that ensures proper blood flow to the intervillous space for fetal nutrition. This process requires the presence of decidual natural killer (dNK) cells, the most numerous cell population at the maternal–fetal interface. Moreover, during interactions with EVT, dNK cells can acquire HLA-G by trogocytosis. Named after the Greek word trogo (to nibble), trogocytosis consists of membrane protein transfer between cells. Despite having been first observed in immune cells in the early 1970s [6], the prevalence and the exact mechanism of trogocytosis are unclear, although some understanding has been obtained [7,8].
The role of trogocytosis in immune surveillance of Hodgkin lymphoma
Published in OncoImmunology, 2020
Consequences of trogocytic transfer of membrane patches are diverse depending on the functions of proteins embedded in these membrane patches. Although trogocytosis has also been reported between many nonimmune cells and even between tumor cells,21,24 trogocytosis has been most commonly observed among immune cells during close cell-cell contacts. This intercellular transfer of membrane patches and proteins contained within them, influences ongoing immune responses. During activation by APCs, ovalbumin-specific CD4+ helper T (Th) cells acquired pMHCI and costimulatory ligands along with pMHCII, and the ability to mimick APCs in stimulating ovalbumin-specific CD8+ T cell responses.25,26 Strikingly, mice receiving this APC-like Th cells as a vaccine, were completely protected from developing lung metastasis caused by tumor cells with this specific antigen.25 However, trogocytosis can also suppress immune responses. During therapeutic antibody treatments for tumors, tumor cells can escape from antibody-dependent cellular phagocytosis and cytotoxicity by Fc receptor-mediated trogocytosis of antigen-antibody complexes.27 HLA-G, an immunosuppressive molecule, has been reported to be transferred among tumor cells and immune cells, leading to a suppressive tumor environment and a dampened anti-tumor immunity.28 Therefore, the effect of trogocytosis on immune responses needs to be analyzed on a case-by-case basis.21 Below, we will summarize recent results on the effect of trogocytosis on HL.