Journal of Undergraduate Research
Keywords
follicular dendritic cells, FDC, CD4+, HIV, CD62L, apoptosis
College
Life Sciences
Department
Microbiology and Molecular Biology
Abstract
Both B and T lymphocytes intimately interact with follicular dendritic cells (FDCs) in lymphoid follicles of secondary lymphoid tissue (e.g., spleen, lymph node, and tonsils). FDCs trap and retain antigens needed to induce and maintain potent memory antibody responses. FDCs contribute both antigen dependent and independent signals to B lymphocytes residing in the microenviroment of germinal centers in secondary lymphoid tissue, which contributes to the optimal activation of these cells as well as T lymphocytes. One important contribution of FDCs to B lymphocytes is signaling that spares these cells from programmed cell death. As B cells differentiate in germinal centers, they begin to mutate the gene segments encoding their antigen receptors. Some of these mutations result in a lowering of the affinity of the receptor for antigen while others leave the affinity unchanged. Importantly, some mutations result in higher affinity interactions between the receptor and antigen. Since antigen specific B cells are important for the ability of the immune system to mount an effective humoral response (antibodies), there needs to be a means for selecting mutations that create high affinity antibodies. This is thought to be accomplished by programming all germinal center B cells to undergo apoptosis unless provided with a rescue signal. The FDC provides the rescue signal and cells are selected based upon their ability to compete for limiting amounts of specific antigen present on FDCs. Those with the highest affinity receptor interact with antigen bearing FDCs and acquire signaling that spares them from apoptosis.
Recommended Citation
Cole, Devon C. and Burton, Dr. Grey
(2014)
"Follicular Dendritic Cells (FDCs) and Sparing of CD4+ T cells from HIV/CD62L Triggered Apoptosis,"
Journal of Undergraduate Research: Vol. 2014:
Iss.
1, Article 828.
Available at:
https://scholarsarchive.byu.edu/jur/vol2014/iss1/828