Control of innate immunity by memory CD4 T cells
TM Strutt, KK McKinstry, SL Swain - Crossroads between Innate and …, 2011 - Springer
TM Strutt, KK McKinstry, SL Swain
Crossroads between Innate and Adaptive Immunity III, 2011•SpringerHow memory CD4 T cells contribute to protection upon pathogen challenge is not fully
understood. Beyond traditional helper functions for CD8 T cell and B cell responses,
memory CD4 T cells can have a potent impact on the character and a magnitude of
inflammatory responses. Here we discuss how memory CD4 T cell control of innate
immunity at early time points after pathogen encounters can influence protective responses.
We also discuss important aspects of the mechanism whereby memory CD4 T cells directly …
understood. Beyond traditional helper functions for CD8 T cell and B cell responses,
memory CD4 T cells can have a potent impact on the character and a magnitude of
inflammatory responses. Here we discuss how memory CD4 T cell control of innate
immunity at early time points after pathogen encounters can influence protective responses.
We also discuss important aspects of the mechanism whereby memory CD4 T cells directly …
Abstract
How memory CD4 T cells contribute to protection upon pathogen challenge is not fully understood. Beyond traditional helper functions for CD8 T cell and B cell responses, memory CD4 T cells can have a potent impact on the character and a magnitude of inflammatory responses. Here we discuss how memory CD4 T cell control of innate immunity at early time points after pathogen encounters can influence protective responses. We also discuss important aspects of the mechanism whereby memory CD4 T cells directly and indirectly impact the activation status of antigen-presenting cells and production of inflammatory cytokines and chemokines from multiple cell types. We suggest that control of innate immune responses by the adaptive immune system is a powerful protective mechanism associated with the memory state and represents an important fail-safe in the face of pathogens that fail to trigger robust inflammatory responses through conserved pattern recognition receptors.
Springer