T cells that mediate cellular immunity can detect the presence of intracellular pathogens, because infected cells display on their surface peptide fragments derived from the pathogen's proteins, so that T cells recognise the peptide MHC molecule complex and kill the infected cells.
Th1 cells mediate cellular immunity and further regulate inflammation responses.
T cells, which mediate cellular immunity, express heterodimeric (αβ or γδ) cell surface receptors (T-cell receptors, or TCRs).
Th1 cells predominantly secrete IFN-γ, IL-12, IL-2, and tumor necrosis factor-α (TNF-α), and mediate cellular immunity, while Th2 cells play a key role in promoting Th1 differentiation and the Th1 response.
Th1 cells produce IL-2, TNF- α, and IFN- γ which mediate cellular immunity, macrophage activation, and cytotoxicity and help in B-cell production of opsonizing and complement fixing antibodies.
Th1 cells are characterized by the production of proinflammatory interferon γ (IFN-γ) to mediate cellular immunity, whereas Th2 cells produce interleukin-4 (IL-4), IL-5, and IL-13, and are responsible for regulating humoral immunity and, in pathological conditions, asthma and allergy.
The results suggested that Th1-mediated cellular immunity in the group immunized with CAV-2-ROP18 is not dependent on IL-10 production during the cellular response against toxoplasmosis.
IFN-γ, which is produced by PCV2-specific IFN-γ-SCs, is a key immunoregulatory cytokine that controls the differentiation of naïve CD4+ into CD4+ cells and mediates cellular immunity against viral infections [ 24].
A classic example is the human major histocompatibility complex molecules of class I (glycoproteins mediating cellular immunity against intracellular pathogens), where all residues under diversifying selection pressure were found clustered in the antigen recognition site [ 38, 39].
Whole cell pertussis vaccine (WCV), which contains abundant LPS, can induce the development of Th1- and Th17-cells in mice that mediate protective cellular immunity to B. pertussis [6], [13].
TLR4 helps to direct the induction of Th1 and Th-17 cells, which mediate protective cellular immunity to B. pertussis.
