Høres jo ut som det kan være vanskelig å ignorere dette faktum dersom man skal lage en vaksine mot Covid 19 da…
Abstract
T cells are central regulators of the immune response and exert their actions by modulating the function of other immune cells and by affecting the behavior of endothelial and parenchymal cells. By expressing membrane-bound molecules and secreting soluble mediators, they control antibody responses, activate innate immune cells, and lyse target cells. Certain T-cell subsets perform suppressive functions and limit the duration of immune responses. Therefore inadequate T-cell function has widespread repercussions for the immune response.
Extensive evidence indicates that T cells are involved in the pathogenesis of systemic lupus erythematosus (SLE.) The phenotype of T cells isolated from patients with SLE is abnormal. Their response to stimulation through the T-cell receptor (TCR) is exaggerated, and their gene expression profile is altered compared with cells obtained from healthy individuals. Moreover, the tolerance breach and self-directed response developed by SLE patients have all the characteristics of a T-cell–driven immune response including clonal expansion and somatic hypermutation, and T-cell depletion prevents lupus in murine models. Thus even though SLE is a complex disease caused by multiple factors, evidence supports the role of T cells as promoters of the pathologic autoimmune response and as direct instigators of target organ damage. The aim of this chapter is to discuss the mechanisms by which T cells contribute to SLE and the intrinsic abnormalities that alter the behavior of the SLE T cell contributing to its pathogenicity.
https://www.sciencedirect.com/topics/medicine-and-dentistry/t-cell