Thanks for that link. CD4 is expressed on helper T cells and it promotes adhesion to antigen-presenting cells.
CD8 is the same but for cytotoxic T cells and different kinds of antigens. CD3 accessory proteins help signal from either of those into helper and cytotoxic cells that something has gone wrong. The helper T cells will help activate an antibody response from B cells and their cytotoxic siblings, and the cytotoxic cells kill off infected cells. I don't know how values across the board would lead to a cytokine storm -- it sounds like immunodeficiency.
On 4/23/20, 2:04 PM, "Friam on behalf of uǝlƃ ☣" <
[hidden email] on behalf of
[hidden email]> wrote:
Suppressed T cell-mediated immunity in patients with COVID-19: A clinical retrospective study in Wuhan, China
https://www.journalofinfection.com/article/S0163-4453(20)30223-1/abstract
Does anyone here have a sense for the types of conditions (cf covid19 comorbidities) that cluster around all 3 proteins? My naive googling returns comments about graft-vs-host and various autoimmune conditions and immunosuppressive therapies. But I'm having trouble getting a feel for how they might all cluster together. Maybe it's simply that lower amounts of *any* of the 3 subsets produces a higher risk for those with covid19? But I keep hearing that the "cytokine storm" is more than just an effect, it may loop back and be part of the problem.
--
☣ uǝlƃ
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