âIâll teach you differencesâ

Lanier, Douglas M.

doi:10.1057/9781137010353.0026

Cited by 5 publications

(5 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The NKG2D/NKG2D ligand system is particularly important to immune surveillance of tumors since expression of NKG2D ligands is induced by carcinogens and stress such as genotoxic stress (29)(30)(31). Human NKG2D ligands consist of two families: MHC class I-related molecules (MICs) and UL16-binding proteins (ULBPs) (16).…”

Section: Discussionmentioning

confidence: 99%

Corticotropin-releasing factor induces immune escape of cervical cancer cells by downregulation of NKG2D

Song

Park

et al. 2014

Oncology Reports

View full text Add to dashboard Cite

Abstract. Corticotropin-releasing factor (CRF), a coordinator of the body's responses to stress, is found in various cancer tissues and cell lines. However, the exact abilities of CRF to manipulate natural killer (NK) cells during immune response have not been studied. NKG2D is an activating receptor that is expressed on most NK and CD8 + T cells. MHC class I-related chain A (MICA) and UL16-binding protein (ULBP) 1, 2 and 3 are well-known ligands for NKG2D. In the present study, we reported our findings regarding the role of CRF in cervical cancer cell survival. Human cervical cancer cell line, HeLa cells, had significantly higher intracellular expression of UL16-binding protein 2 (ULBP2) following CRF treatment but had only slightly increased surface expression of ULBP2. Notably, MMPi (pan-metalloproteases inhibitor) blocked the release of ULBP2 molecules from the surface of HeLa cells. Furthermore, incubating NK cells with culture supernatants from CRF-treated HeLa cells, which contained soluble NKG2D ligand, reduced NK cell activity by decreasing surface expression of NKG2D. Collectively, downregulation of NKG2D by CRF-induced soluble NKG2D ligand provides a potential mechanism by which cervical cancer cells escape NKG2D-mediated attack under stress conditions.

show abstract

Section: Discussionmentioning

confidence: 99%

Corticotropin-releasing factor induces immune escape of cervical cancer cells by downregulation of NKG2D

Song

Park

et al. 2014

Oncology Reports

View full text Add to dashboard Cite

show abstract

“…All told, many anatomical education commentators broadly welcome the increased use of technologies in anatomy education (Drake et al, 2009; Rizzolo et al, 2010), with some highlighting the value of AI in particular (Sugand et al, 2010; Trelease, 2016; Guimarães et al, 2017; McBride & Drake, 2018). Nonetheless, these discussions all too often fail to engage with the burgeoning literature raising concerns about the social impacts of AI (Eubanks, 2018; Benjamin, 2019; Pasquale, 2019; Katz, 2020; Lanier & Weyl, 2020; Chun, 2021). Incorporating AI into anatomy education may therefore provide unique benefits, but there may also be unintended consequences.…”

Section: Strengths and Opportunities With Artificial Intelligence‐inf...mentioning

confidence: 99%

Artificial intelligence and clinical anatomical education: Promises and perils

Lazarus

Truong

Douglas

et al. 2022

Anatomical Sciences Ed

View full text Add to dashboard Cite

Anatomy educators are often at the forefront of adopting innovative and advanced technologies for teaching, such as artificial intelligence (AI). While AI offers potential new opportunities for anatomical education, hard lessons learned from the deployment of AI tools in other domains (e.g., criminal justice, healthcare, and finance) suggest that these opportunities are likely to be tempered by disadvantages for at least some learners and within certain educational contexts. From the perspectives of an anatomy educator, public health researcher, medical ethicist, and an educational technology expert, this article examines five tensions between the promises and the perils of integrating AI into anatomy education. These tensions highlight the ways in which AI is currently ill‐suited for incorporating the uncertainties intrinsic to anatomy education in the areas of (1) human variations, (2) healthcare practice, (3) diversity and social justice, (4) student support, and (5) student learning. Practical recommendations for a considered approach to working alongside AI in the contemporary (and future) anatomy education learning environment are provided, including enhanced transparency about how AI is integrated, AI developer diversity, inclusion of uncertainty and anatomical variations within deployed AI, provisions made for educator awareness of AI benefits and limitations, building in curricular “AI‐free” time, and engaging AI to extend human capacities. These recommendations serve as a guiding framework for how the clinical anatomy discipline, and anatomy educators, can work alongside AI, and develop a more nuanced and considered approach to the role of AI in healthcare education.

show abstract

“…While most of the CD 16 * cells are CD3 large granular lymphocytes, a small fraction of CD3T cells have also been reported to express CD 16 [19]. To determine if this CD3-CD16-population has NK activity that can be induced by these antibodies, effector cells were separated into CD3* and CD3 populationsand tested with 9-1 and 3G8 ( the positive selection of CD3* cells induced killing in some experiments.…”

Section: Characterization Of the Effector Celt Populations Induced Bymentioning

confidence: 99%

Agonistic Effects of Anti‐CD2 and Anti‐CD16 Antibodies on Human Natural Killer Killing

et al. 1989

View full text Add to dashboard Cite

Two monoclonal antibodies (MoAb), 9-1 (anti-CD2) and 3G8 (anti-CD16), were previously shown to enhance the cytotoxic activity of human natural killer (NK) cells. The present study examined the effect of 9-1 and 3G8 with different effector and target cells to determine whether they activate NK cells through a common mechanism. Analysis of purified lymphocyte subpopulations demonstrated that the CD3+CD16+CD3- NK effector cell population is enhanced by both antibodies, while purified CD2+CD16-CD3+ T cells are not activated by either antibody. Although both antibodies enhance killing of K-562 and Daudi, killing of T-cell lines is enhanced by 9-1 and inhibited by 3G8. In contrast, killing of the promyelocytic cell line, U-937 is inhibited by 9-1 and enhanced by 3G8. On NK-susceptible cells the pattern of enhancement with 3G8, an IgG1 MoAb, is consistent with the pattern of target cell expression of an Fc receptor, FcR II, known to bind IgG1 antibodies. This suggests that 3G8 may cross-link effector and target cells through CD16 on the effectors and FcR II on these targets. This could activate NK killing by a mechanism similar to antibody-dependent cellular cytotoxicity reactions (ADCC) with the MoAb in the reverse orientation. The failure of 3G8 F(ab')2 fragments to enhance NK killing, further supports the reverse ADCC mechanism of enhancement by 3G8. The pattern of enhancement mediated by 9-1, an IgG3 MoAb, is not correlated with any target cell Fc-receptor known to bind IgG3 MoAb. The effect of 9-1 may result, instead, from its binding to the unique 9-1 epitope on the CD2 molecule involved in CD2-mediated T-cell activation, as previously described. Alternative mechanisms, including activation of NK killing by 9-1 mediated cross-linking of CD2 and CD16 on the effector cells, have also been discussed.

show abstract

âIâll teach you differencesâ

Cited by 5 publications

References 0 publications

Corticotropin-releasing factor induces immune escape of cervical cancer cells by downregulation of NKG2D

Corticotropin-releasing factor induces immune escape of cervical cancer cells by downregulation of NKG2D

Artificial intelligence and clinical anatomical education: Promises and perils

Agonistic Effects of Anti‐CD2 and Anti‐CD16 Antibodies on Human Natural Killer Killing

Contact Info

Product

Resources

About

âIâll teach you differencesâ

Cited by 5 publications

References 0 publications

Corticotropin-releasing factor induces immune escape of cervical cancer cells by downregulation of NKG2D

Corticotropin-releasing factor induces immune escape of cervical cancer cells by downregulation of NKG2D

Artificial intelligence and clinical anatomical education: Promises and perils

Agonistic Effects of Anti‐CD2 and Anti‐CD16 Antibodies on Human Natural Killer Killing

Contact Info

Product

Resources

About

âIâll teach you differencesâ