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Related Concept Videos

T Cell Activation and Clonal Selection01:22

T Cell Activation and Clonal Selection

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T cells are integral to our adaptive immune system, recognizing and effectively responding to foreign antigens. T cell activation and clonal selection are pivotal in orchestrating this immune response. This article elucidates these mechanisms, detailing the roles of cluster of differentiation (CD) markers, major histocompatibility complex (MHC) molecules, costimulatory signals, and the process of clonal selection.
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When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
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The adaptive immune system, a crucial component of the overall immune response, offers a highly specialized defense against pathogens. It involves specific cell types and features, enabling it to combat infections effectively and efficiently.
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The T and B lymphocytes of the adaptive immune system develop from common lymphoid progenitor cells in the bone marrow. These progenitors give rise to precursors that eventually develop into both T and B lymphocytes. As these precursors mature, they gain the ability to detect and respond to foreign antigens in the body, a process known as immunocompetence. Additionally, these precursors acquire self-tolerance, a process that ensures they do not react to self-antigens. This intricate system...
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Cytotoxic T Cells-mediated Immune Response01:27

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Cytotoxic T cells are a vital component of the immune system. They have the remarkable ability to identify and target antigens on infected or abnormal cells. These antigens often originate from intracellular pathogens such as viruses or abnormal proteins cancer cells produce.
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Generation of Human Chimeric Antigen Receptor Regulatory T Cells
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Belatacept-Resistant Rejection Is Associated With CD28+ Memory CD8 T Cells.

D V Mathews1, W C Wakwe1, S C Kim1

  • 1Emory Transplant Center, Atlanta, GA.

American Journal of Transplantation : Official Journal of the American Society of Transplantation and the American Society of Transplant Surgeons
|May 15, 2017
PubMed
Summary
This summary is machine-generated.

Belatacept therapy for kidney transplants shows increased rejection linked to specific T cells. These CD28+ CD8+ T_EMRA cells resist belatacept, highlighting a need for targeted therapies to improve transplant outcomes.

Keywords:
animal models: nonhuman primatebasic (laboratory) research/sciencecostimulationfusion proteins and monoclonal antibodies: belataceptfusion proteins and monoclonal antibodies: costimulation molecule specificimmunobiologyimmunosuppressantimmunosuppression/immune modulationrejection: T cell mediated (TCMR)

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Area of Science:

  • Immunology
  • Transplantation immunology
  • T cell biology

Background:

  • Novel immunosuppressive therapies aim to improve transplant efficacy and reduce toxicity.
  • Belatacept, a CD28-CD80/86 inhibitor, offers benefits but is linked to higher rejection rates.
  • Understanding belatacept-associated rejection mechanisms is crucial for its wider clinical use.

Purpose of the Study:

  • To investigate the mechanisms underlying kidney transplant rejection in nonhuman primates treated with belatacept versus tacrolimus.
  • To identify specific immune cell populations associated with belatacept-mediated rejection.

Main Methods:

  • A nonhuman primate kidney transplant model was utilized.
  • Animals received either a belatacept-based or a tacrolimus-based immunosuppressive regimen.
  • Pre-transplant and post-transplant immune cell frequencies, including CD28+ CD8+ T_EMRA cells, were analyzed.

Main Results:

  • Elevated pre-transplant CD28+ CD8+ T_EMRA cell frequencies correlated with rejection in belatacept-treated animals, but not in tacrolimus-treated ones.
  • In rejecting allografts, CD28+ CD8+ T_EMRA cells rapidly lost CD28 expression post-transplant, with CD28- cells dominating the infiltrate.
  • These findings suggest CD28+ memory T cells may be resistant to belatacept and can differentiate while retaining effector function.

Conclusions:

  • CD28+ memory T cells exhibit resistance to belatacept therapy.
  • These cells undergo differentiation, including CD28 loss, while maintaining effector function.
  • Targeted therapies addressing the unique signaling of CD28+ memory T cells could synergize with belatacept to prevent costimulation-independent rejection.