ICOSL-dependent T-cell co-stimulation contributes to the host defense against herpesvirus infections, and accordingly, these pathogens have developed immune evasion mechanisms to interrupt the ICOSL:ICOS signaling pathway.
TCR and CD40L microclusters are linked in synaptic ectosomes (extracellular vesicles) and released in the immunological synapse by helper T cells and induce dendritic cell maturation and cytokine production.
Intersectin2 deficiency is associated with impaired humoral responses to viral infection and B-cell-intrisic defects in germinal centre formation, resulting from the reduced ability of intersectin2-KO B cells to establish cognate interactions with helper T cells.
Cancer cell expression of the T-cell co-stimulatory molecule CD80, or treatment with agonistic antibodies targeting the T-cell co-stimulatory receptors OX-40 or 4-1BB, enhances the anti-tumor activity of FAK inhibition.
Immune expulsion of helminth parasites is driven by two key pathways mediated by soluble cytokines ligating to the IL-4 and IL-25 receptors acting on innate effector cells throughout the course of infection.