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Updated: Oct 17, 2025

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Increased CD47 and MHC Class I Inhibitory Signals Expression in Senescent CD1 Primary Mouse Lung Fibroblasts.

Elisa Hernández-Mercado1,2, Jessica Lakshmi Prieto-Chávez3, Lourdes Andrea Arriaga-Pizano3

  • 1Laboratorio de Bioenergetica y Envejecimiento Celular, Departamento de Ciencias de la Salud, Universidad Autónoma Metropolitana-Iztapalapa, Mexico City 09340, Mexico.

International Journal of Molecular Sciences
|October 13, 2021
PubMed
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Senescent cells evade immune clearance by increasing CD47 and MHC-I signals. These changes in cellular senescence may hinder the immune system

Area of Science:

  • Cellular biology
  • Immunology
  • Gerontology

Background:

  • Cellular senescence is a biological state with crucial roles in tissue homeostasis.
  • Accumulation of senescent cells contributes to aging and age-related diseases.
  • The immune system's role in clearing senescent cells is not fully understood.

Purpose of the Study:

  • To investigate the expression of CD47, MHC-I, and calreticulin on senescent cells.
  • To determine if these molecules are involved in evading immune clearance.

Main Methods:

  • Induction of stress-induced premature senescence (SIPS) and replicative senescence (RS) in primary mouse lung fibroblasts.
  • Analysis of CD47, MHC-I, and calreticulin expression on senescent cells.
Keywords:
CD47MHC class Icalreticulinsenescent cell clearance regulation

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Main Results:

  • Senescent fibroblasts (both RS and SIPS) showed a significant increase in CD47 and MHC-I.
  • Calreticulin expression remained unchanged in senescent cells.
  • These findings suggest a mechanism for senescent cells to avoid immune detection.

Conclusions:

  • Increased CD47 and MHC-I on senescent cells may facilitate immune evasion.
  • Understanding these mechanisms is crucial for targeting senescent cells in aging and disease.
  • Further research is needed to explore the precise roles of these signals in immune clearance.