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CD8 T cell memory in B cell-deficient mice

M S Asano1, R Ahmed

  • 1Department of Microbiology and Immunology, University of California at Los Angeles School of Medicine 90024, USA.

The Journal of Experimental Medicine
|May 1, 1996
PubMed
Summary

B cells and antibodies are not essential for generating or maintaining CD8+ cytotoxic T lymphocyte (CTL) memory. This study shows that CTL memory persists effectively in B cell-deficient mice, ensuring robust responses upon reinfection.

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Area of Science:

  • Immunology
  • T cell memory
  • B cell function

Background:

  • Antigen presentation by B cells and antigen-antibody complexes on follicular dendritic cells (FDCs) are thought to sustain T cell memory.
  • The specific role of B cells and antibodies in CD8+ cytotoxic T lymphocyte (CTL) memory generation and maintenance remains to be fully elucidated.

Purpose of the Study:

  • To investigate the necessity of B cells and antibodies for the generation and long-term maintenance of CD8+ CTL memory.
  • To compare CTL responses to lymphocytic choriomeningitis virus (LCMV) in normal versus B cell-deficient mice across different phases of the immune response.

Main Methods:

  • Comparison of CTL responses to acute LCMV infection in normal (+/+) and B cell-deficient mice.
  • Analysis of CTL response phases: expansion, death, and long-term memory.
  • Quantification of virus-specific CD8+ T cells and activated CD8+ T cells, and assessment of CTL killing activity.

Main Results:

  • B cells are not required for the expansion and activation of virus-specific CTL; effector CTL response kinetics and magnitude are identical in both groups.
  • While the 'death' phase of CTLs is more pronounced in B cell-deficient mice, the frequencies of LCMV-specific CTLs remain comparable.
  • The long-term memory phase of CTL response is unaffected by the absence of B cells, with stable CTL numbers persisting for up to 6 months.
  • B cell-deficient mice that resolved LCMV infection exhibit accelerated CTL responses and efficient viral clearance upon reinfection, indicating intact CTL memory.

Conclusions:

  • Neither B cells nor antigen-antibody complexes are essential for the maintenance of CD8+ CTL memory.
  • CTL memory, assessed by frequency or protective immunity, is not diminished in the absence of B cells.
  • The findings challenge the established role of B cells and antibody complexes in sustaining long-term T cell memory.

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