کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5546171 | 1555900 | 2017 | 5 صفحه PDF | دانلود رایگان |
- HIV disease damages germinal centers and biases immunity towards alternate pathways.
- Canonical B cell maturation can occur in the absence of germinal centers.
- Extrafollicular humoral immunity is more robust than previously thought.
- KSHV lymphoproliferations are associated with extrafollicular B cell maturation.
Early events in the pathogenesis of KSHV-associated lymphoproliferations in the context of HIV disease remain poorly understood. Recent research indicates that latent HIV infection causes persistent immune dysfunction in B cell follicles. Simultaneously, lack of T cell immune surveillance in the lymph nodes dysregulates the biology of EBV. In sum, these defects bias B lymphocyte maturation away from traditional T cell-dependent germinal center-mediated pathways and towards extrafollicular pathways. Recent advances in B lymphocyte immunology suggest that extrafollicular maturation pathways for antibody secreting cells are more flexible and robust than previously believed. These responses are now understood to be both durable and antigen-specific, and even canonically germinal center-restricted events such as class switch recombination and somatic hypermutation have now been demonstrated in an extrafollicular context. As a lymphotrophic pathogen which causes disease primarily in the context of HIV and EBV co-infection, future studies examining the interactions of KSHV biology with extrafollicular B cell maturation pathways will be critical to uncovering key aspects of KSHV-mediated immune pathology.
Journal: Current Opinion in Virology - Volume 26, October 2017, Pages 69-73