Abstract
Fibrotic tissue involution occurs in a large variety of chronic diseases. As the final phase of follicular atrophy and depletion, a diffuse fibrosis is the more severe consequence of the chronic process of lymph node involution that characterizes HIV infection. This review focuses on the comparison between HIV-induced lymph node fibrosis and other chronic fibroproliferative diseases, in terms of cell types participating in the process and signaling intermediates that together cause the deposition of collagen and remodel normal tissue architecture. Given that the histological quantification of this type of fibrosis cannot be easily introduced as a routine method in clinical pathology, we will discuss the possibility of exploiting some functional modifications, which express the adaptation of T cells to the fibrotic/hypoxic environment, as biochemical markers of the evolution of lymph node damage.
Financial & competing interests disclosure
Giuseppa Visalli is the recipient of a Fellowship from the University of Messina. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
No writing assistance was utilized in the production of this manuscript.
Notes
Physiologically, energy production ensures main housekeeping functions and protein quality control. Thus, new protein synthesis and ubiquitination of proteins destined for degradation are strictly ATP-dependent processes. This interdependence between ATP production and housekeeping function is particularly evident in T cells activated by mitogens in culture. When analyzed as paradigmatic models of energy-consuming biochemical processes, the decline of these functions is a typical example of how the activation of lymphocytes from patients occurs with low levels of energy consumption.