In COVID-19, antigen size lower or larger than 70 kDa modulates the sepsis and memory B cells

This review pretends to shed light on the immune processes occurring in coronavirus disease 2019 (COVID-19) from a perspective based antigens size, lower or larger than 70 kDa. cutoff size point explains host type of response against antigenic proteins severe acute respiratory syndrome 2 (SARS-CoV-2), which may lead development memory B cells or, conversely, suppression, apoptosis, viral escape, and sepsis. Here, previous experimental work related literature, following is proposed: < kDa can access germinal center through follicular conduits, where activated present processed antigen specific naive CD4+ T that, interaction with major histocompatibility complex class II (MHC-II), trigger helper (Th2). Conversely, > cannot circulate narrow conduits network might be captured within subcapsular sinus by macrophages dendritic cells. Then, these cognate are presented, via complement receptors, that acquire them MHC-II cells, triggering Th1. The sustained infected lysis overfeed high levels unassembled kDa, strong persistent cell receptor (BCR) activation, enhancing Th2 response, releasing interleukin-10 (IL-10) transforming growth factor-beta (TGF-β) paralysis, sepsis, death. Finally, it suggested polymerization into an polymer could shift Th1, developing immunoglobulin G2 (IgG2) production, avoiding