Human natural killer cell immunophenotyping-strategy to predict donor killing capacity

Presenter Type

UNO Undergraduate Student

Major/Field of Study

Biology

Advisor Information

Dr. Paul W. Denton

Location

MBSC Ballroom Poster # 506 - U

Presentation Type

Poster

Start Date

24-3-2023 1:00 PM

End Date

24-3-2023 2:15 PM

Abstract

Natural killer (NK) cells are a component of the innate immune system that kill target cells in a similar fashion to how cytotoxic T lymphocytes kill target cells within the adaptive immune system. NK cells kill malignant or infected targets in one of two ways: direct killing or antibody dependent cellular cytotoxicity (ADCC). NK cells can be stimulated by immunotherapies or by a disease condition. Upon stimulation, NK cells undergo changes to their surface – specifically, the changes are to the types and/or frequencies of surface markers present on the cells. These changes are “phenotypes” that we can recognize as “immunophenotypes” using fluorescently labeled antibodies and a flow cytometer as our detector. But more importantly, from a physiological perspective, these cell surface changes represent alterations in signaling within the cells that leads them to gain the capacity to mediate cytotoxicity against target cells. As NK cells are stimulated, the NK cells express different surface markers over time, changing their immunophenotype as the markers change. Recently our lab has developed an assay to look simultaneously at direct killing and ADCC while using various immunotherapies. In parallel, we have also developed an immunophenotyping panel to look at the composition of surface markers on the NK cells used in the killing tests. This project aims to inspect the relationship between donor NK immunophenotypes and their killing capacity in both ADCC and direct killing. Data-to-date will be presented. Our ambition is to develop our immunophenotyping-strategy to be clinically viable as a predictive efficacy screening tool for physicians to utilize prior to prescribing certain therapies (e.g., immunotherapies) in patients.

Scheduling

1-2:15 p.m., 2:30 -3:45 p.m.

This document is currently not available here.

COinS
 
Mar 24th, 1:00 PM Mar 24th, 2:15 PM

Human natural killer cell immunophenotyping-strategy to predict donor killing capacity

MBSC Ballroom Poster # 506 - U

Natural killer (NK) cells are a component of the innate immune system that kill target cells in a similar fashion to how cytotoxic T lymphocytes kill target cells within the adaptive immune system. NK cells kill malignant or infected targets in one of two ways: direct killing or antibody dependent cellular cytotoxicity (ADCC). NK cells can be stimulated by immunotherapies or by a disease condition. Upon stimulation, NK cells undergo changes to their surface – specifically, the changes are to the types and/or frequencies of surface markers present on the cells. These changes are “phenotypes” that we can recognize as “immunophenotypes” using fluorescently labeled antibodies and a flow cytometer as our detector. But more importantly, from a physiological perspective, these cell surface changes represent alterations in signaling within the cells that leads them to gain the capacity to mediate cytotoxicity against target cells. As NK cells are stimulated, the NK cells express different surface markers over time, changing their immunophenotype as the markers change. Recently our lab has developed an assay to look simultaneously at direct killing and ADCC while using various immunotherapies. In parallel, we have also developed an immunophenotyping panel to look at the composition of surface markers on the NK cells used in the killing tests. This project aims to inspect the relationship between donor NK immunophenotypes and their killing capacity in both ADCC and direct killing. Data-to-date will be presented. Our ambition is to develop our immunophenotyping-strategy to be clinically viable as a predictive efficacy screening tool for physicians to utilize prior to prescribing certain therapies (e.g., immunotherapies) in patients.