1998TransplantationRequires access

C1.7 MONOCLONAL ANTIBODY DESIGNATES HIGH-AVIDITY CD4+ CYTOTOXIC T LYMPHOCYTES INVOLVED IN CLINICAL HEART REJECTION

Nancy E.M. van Emmerik, Christiaan J. Knoop, Leonard M.B. Vaessen, Aggie H.M.M. Balk, B. Mochtar, Frans H.J. Claas, Willem Weimar

Open publisher page 11 citations

Abstract

BACKGROUND: It is assumed that not all donor-specific cytotoxic T lymphocytes (CTLs), but only those with a high avidity for donor antigens, can function as terminal effector cells in transplant rejection. METHODS: In the present study, we searched for markers that would exclusively designate these high-avidity CTL. RESULTS: FACS analysis of donor-specific CTL clones obtained from heart transplant patients revealed that high- and low-avidity CTL varied in their expression of p38, a surface molecule involved in signal transduction, which is stained by the antibody C1.7. High- and low-avidity CD8+ CTL and high-avidity CD4+ CTL expressed p38, whereas low-avidity CD4+ CTL did not. Noncytotoxic and naive CD4+ lymphocytes also lacked p38 surface expression. CONCLUSION: Therefore, we conclude that p38 is a marker for CD4+ lymphocytes with the potency to damage the transplanted heart. Accordingly, p38 might be used to analyze the contribution of CD4+ CTL in immune responses, such as transplant rejection.

About this research paper

What this paper is about

BACKGROUND: It is assumed that not all donor-specific cytotoxic T lymphocytes (CTLs), but only those with a high avidity for donor antigens, can function as terminal effector cells in transplant rejection. METHODS: In the present study, we searched for markers that would exclusively designate these high-avidity CTL. RESULTS: FACS analysis of donor-specific CTL clones obtained from heart transplant patients revealed that high- and low-avidity CTL varied in their expression of p38, a surface molecule involved in signal transduction, which is stained by the antibody C1.7. High- and low-avidity CD8+ CTL and high-avidity CD4+ CTL expressed p38, whereas low-avidity CD4+ CTL did not. Noncytotoxic and naive CD4+ lymphocytes also lacked p38 surface expression. CONCLUSION: Therefore, we conclude that p38 is a marker for CD4+ lymphocytes with the potency to damage the transplanted heart. Accordingly, p38 might be used to analyze the contribution of CD4+ CTL in immune responses, such as transplant rejection.

Why it matters

OpenAlex reports 11 citations for this work. Citation counts describe recorded attention and do not establish research quality.

Key contribution

A contribution statement is not available in the OpenAlex record.

Method / approach

Method details are not available in the OpenAlex metadata.

Main findings

Findings are not separately available in the OpenAlex metadata.

Limitations

Limitations are not available in the OpenAlex metadata.

Applications

Application details are not available in the OpenAlex metadata.

Available abstract

BACKGROUND: It is assumed that not all donor-specific cytotoxic T lymphocytes (CTLs), but only those with a high avidity for donor antigens, can function as terminal effector cells in transplant rejection. METHODS: In the present study, we searched for markers that would exclusively designate these high-avidity CTL. RESULTS: FACS analysis of donor-specific CTL clones obtained from heart transplant patients revealed that high- and low-avidity CTL varied in their expression of p38, a surface molecule involved in signal transduction, which is stained by the antibody C1.7. High- and low-avidity CD8+ CTL and high-avidity CD4+ CTL expressed p38, whereas low-avidity CD4+ CTL did not. Noncytotoxic and naive CD4+ lymphocytes also lacked p38 surface expression. CONCLUSION: Therefore, we conclude that p38 is a marker for CD4+ lymphocytes with the potency to damage the transplanted heart. Accordingly, p38 might be used to analyze the contribution of CD4+ CTL in immune responses, such as transplant rejection.

Key concepts: Avidity, CTL*, Cytotoxic T cell, CD8, Immunology, Monoclonal antibody, Antibody, Biology

Related papers

Back to paper searchBrowse research topicsOriginal source
C1.7 MONOCLONAL ANTIBODY DESIGNATES HIGH-AVIDITY CD4+ CYTOTOXIC T LYMPHOCYTES INVOLVED IN CLINICAL HEART REJECTION — Research Paper | ScholarLens