CD8+ T-cell immunity orchestrated by iNKT cells

Abstract

CD8+ T cells belonging to the adaptive immune system play key roles in defending against viral infections and cancers. The current CD8+ T cell-based immunotherapy has emerged as a superior therapeutic avenue for the eradication of tumor cells and long-term prevention of their recurrence in hematologic malignancies. It is believed that an effective adaptive immune response critically relies on the help of the innate compartment. Invariant natural killer T (iNKT) cells are innate-like T lymphocytes that have been considered some of the first cells to respond to infections and can secrete a large amount of diverse cytokines and chemokines to widely modulate the innate and adaptive immune responders. Like CD8+ T cells, iNKT cells also play an important role in defense against intracellular pathogenic infections and cancers. In this review, we will discuss the CD8+ T-cell immunity contributed by iNKT cells, including iNKT cell-mediated cross-priming and memory formation, and discuss recent advances in our understanding of the mechanisms underlying memory CD8+ T-cell differentiation, as well as aging-induced impairment of T-cell immunity.

Evaluating the link between immune characteristics and attention deficit hyperactivity disorder through a bi-directional Mendelian randomization study

“…NKT cells uniquely contribute to enhancing CD8 T-cell priming and secondary reactions, or they control the destiny of CD8 T-cells (be it death or memory formation) through their interaction timing, location, and specific NKT cell groups. Furthermore, age-related alterations in the quantity and roles of NKT cells are notable, with scant studies indicating that these cells hinder T-cell immune responses ( 56 ).…”

Recombinant antigen P29 of Echinococcus granulosus induces Th1, Tc1, and Th17 cell immune responses in sheep

“…CD4 + T cells recognize MHC-II antigen molecules, mainly by promoting antigen presentation and upregulating co-stimulatory molecules on dendritic cells to induce a strong CD8 + T cell response (25, 26). CD8 + T cells recognize MHC-I molecules and can differentiate into cytotoxic cells capable of resisting pathogenic invasion (27,28). Treatment of chronic Toxoplasma gondii infection with antigenspecific undepleted CD4 + T cells restores CD8 + T cell function in the host and prevents potential reinfection, suggesting that CD8 + T cells require the help of CD4 + T cells (29).…”

Protein Citrullination by Peptidyl Arginine Deiminase/Arginine Deiminase Homologs in Members of the Human Microbiota and Its Recognition by Anti-Citrullinated Protein Antibodies

“…It has been proposed that when this mutualistic relationship is impaired by dysbiotic events, dysregulated local and systemic immune responses occur [17,18]. The mechanisms that connect intestinal dysbiosis with autoimmune pathways involve: Dysfunction of intestinal dendritic cells [19], innate lymphoid cells [20], and mechanisms related to phagocytic function [21], alteration in intestinal mast cell density, C macrophage activation [22], damage to the intestinal epithelial barrier, imbalance of CD4+ cells, depletion of CD8+ cells, alteration in the marginal B-cell zone, dysfunction of plasmacytoid DCs, and invariant natural killer cells [23]. The decrease in butyrate derived from the microbiota reduces cellular metabolism, affects the memory of activated CD8+ T cells, and impairs optimal recovery responses after antigen re-encounter [24].…”