Journal
FRONTIERS IN IMMUNOLOGY
Volume 12, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fimmu.2021.677036
Keywords
memory; CD4 lymphocyte; gene regulation; longevity; B cell Ag presentation; new CD4 memory markers; resting memory CD4+T-cells
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Funding
- NIAID [R01AI063764, R21AI101987, R01AI120634]
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Dendritic cells are important antigen presenting cells that activate the immune system, while B cell antigen presentation, though less prominent, is crucial for the formation and maintenance of memory CD4 T cells. Low levels of antigens captured by B cells during resolution of infection can induce a quiescent state in memory CD4 T cells, contributing to their long-term survival. This mechanism may be necessary to prevent autoimmunity and cross-reactivity to autoantigens.
Dendritic cells are the antigen presenting cells that process antigens effectively and prime the immune system, a characteristic that have gained them the spotlights in recent years. B cell antigen presentation, although less prominent, deserves equal attention. B cells select antigen experienced CD4 T cells to become memory and initiate an orchestrated genetic program that maintains memory CD4 T cells for life of the individual. Over years of research, we have demonstrated that low levels of antigens captured by B cells during the resolution of an infection render antigen experienced CD4 T cells into a quiescent/resting state. Our studies suggest that in the absence of antigen, the resting state associated with low-energy utilization and proliferation can help memory CD4 T cells to survive nearly throughout the lifetime of mice. In this review we would discuss the primary findings from our lab as well as others that highlight our understanding of B cell antigen presentation and the contributions of the MHC Class II accessory molecules to this outcome. We propose that the quiescence induced by the low levels of antigen presentation might be a mechanism necessary to regulate long-term survival of CD4 memory T cells and to prevent cross-reactivity to autoantigens, hence autoimmunity.
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