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Related Concept Videos

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Cell-mediated Immune Responses

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Immune Response Against Viral Pathogens

The immune system's response to viral infections is a complex and coordinated process involving natural killer (NK) cells, T cell-mediated responses, and antibody-mediated responses.
NK Cells
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An antigen is any substance the immune system identifies as foreign and potentially harmful to the body, prompting an immune response. Antigens have two functional properties: immunogenicity and reactivity. Immunogenicity is the ability of an antigen to stimulate a specific immune response. At the same time, reactivity describes the antigen's ability to react with the cells and antibodies produced in response to it.
Complete Antigens
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Heterologous immunity triggered by a single, latent virus in Mus musculus: combined costimulation- and adhesion-

Jonathan M Beus1, Salila S Hashmi, Saranya A Selvaraj

  • 1Emory Transplant Center, Emory University School of Medicine, Atlanta, Georgia, United States of America.

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|August 14, 2013
PubMed
Summary
This summary is machine-generated.

Latent MHV68 infection accelerates transplant rejection by altering T cell responses. Combining anti-CD154 with adhesion blockade overcomes this rejection, suggesting dual pathway targeting is key for managing virus-mediated alloimmunity.

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Area of Science:

  • Immunology
  • Transplantation Biology
  • Virology

Background:

  • Latent viruses can influence immune responses, potentially impacting transplant outcomes.
  • Mechanisms of latent virus-mediated heterologous immunity and transplant rejection, particularly with T cell costimulation blockade, are not fully understood.
  • Murine herpesvirus 68 (MHV68) serves as a model for studying latent viral infections.

Purpose of the Study:

  • To investigate the mechanisms of latent virus-induced heterologous alloimmunity and transplant rejection.
  • To determine the efficacy of combined immunotherapies in overcoming virus-mediated transplant rejection.
  • To elucidate the role of T cell costimulation and adhesion molecules in this context.

Main Methods:

  • Development of a rodent model using MHV68 for latent virus-induced heterologous alloimmunity.
  • Analysis of immune deviations, including cytokine secretion (CXCL9, CXCL10) and CD8 T cell populations.
  • Assessment of skin allograft rejection under various blockade strategies: costimulation blockade (CTLA-4-Ig/anti-CD154) and adhesion blockade (anti-LFA-1/anti-VLA-4).

Main Results:

  • MHV68 infection led to immune deviation, characterized by increased CXCL9/10 and CD8(dim) T cells with altered costimulation and adhesion molecule expression.
  • Infected recipients showed accelerated, costimulation blockade-resistant skin allograft rejection.
  • Combined anti-CD154 and anti-LFA-1/anti-VLA-4 blockade prolonged graft acceptance in infected animals, unlike costimulation blockade alone.
  • Synergy between adhesion pathways and CD154-based costimulation was crucial for overcoming MHV68-induced rejection.

Conclusions:

  • Latent MHV68 infection promotes alloimmune responses that resist standard costimulation blockade.
  • Targeting both adhesion molecules (LFA-1, VLA-4) and CD154-mediated costimulation is essential to prevent transplant rejection in the context of latent viral infections.
  • These findings highlight the importance of considering viral latency in transplantation and suggest novel therapeutic strategies.