Effector Mechanisms of T Cell-Mediated Immunity

Flashcards covering the mechanisms of T cell-mediated immunity, including CD4+ and CD8+ effector functions, T cell subsets (Th1, Th2, Th17, Treg), and microbial evasion strategies.

Cell-Mediated Immunity (CMI)

Immune reactions that eliminate different types of microbes through two main types: CD4 Th cells that recruit/activate leukocytes and CD8 CTLs that directly kill infected cells.

CD4 Th Cells

T cells that express molecules to recruit and activate other leukocytes, such as macrophages, to phagocytose and destroy microbes.

CD8 CTL (Cytotoxic T Lymphocytes)

Effector cells that directly kill infected cells containing microbial proteins in the cytosol or cancer cells; they also produce cytokines that induce inflammation and activate macrophages.

Treg Cells

Effector cells that inhibit T-cell responses to control immune reactions and prevent autoimmunity by secreting TGFβ, IL-10, and IL-35.

Signal 3

The 'driving cytokine(s)' produced by DCs and other cells in response to different microbes that drive the differentiation of antigen-activated T cells into specific subsets.

Th1 Cells

A subset of CD4+ T cells that produces IFN-γ to activate M1 macrophages for the destruction of intracellular microbes; they utilize transcription factors Stat1, Stat4, and T-bet.

IFN-γ (Interferon-gamma)

The signature cytokine of Th1 cells and a potent macrophage-activating cytokine that enables macrophages to destroy intracellular microbes more efficiently.

M1 Macrophages (Classical)

Macrophages induced by microbial products binding to TLRs and IFN-γ; they are microbicidal, pro-inflammatory, and produce ROS, NO, and lysosomal enzymes.

Th2 Cells

A subset of CD4+ T cells induced by helminthic parasite infections that produces IL-4, IL-5, and IL-13 to promote IgE and eosinophil-mediated destruction; they utilize transcription factors Stat6 and GATA3.

M2 Macrophages (Alternative)

Macrophages induced by IL-4 and IL-13 that are important in tissue repair, collagen synthesis, and fibrosis, while also inhibiting classical macrophage activation.

Th17 Cells

A subset of CD4+ T cells that develops in response to extracellular bacterial and fungal infections; they produce IL-17 to recruit neutrophils and monocytes and utilize transcription factors Stat3 and RORγt.

FOXP3

The transcription factor induced in the presence of TGFβ alone (and absence of pro-inflammatory cytokines) that leads to the development of Treg cells.

Psoriasis

An inflammatory disease in which Th17 cells are implicated; it is treated with antagonists that neutralize IL-12 and IL-23.

Fas (CD95)

A death-inducing receptor expressed on the surface of target cells, such as virally infected cells or tumor cells.

Fas Ligand (FasL, CD178)

A transmembrane protein expressed on activated CTLs and NK cells that binds to Fas on target cells to activate caspases and induce apoptosis.

Perforin

A granule protein released by CTLs that allows for the delivery of granzymes into the cytosol of a target cell.

Granzymes

Granule enzymes released by CTLs that cleave and activate caspases present in the cytosol of the target cell to induce apoptosis.

T cell exhaustion

The premature termination of CTL effector function, typically occurring in response to chronic antigenic stimulation and characterized by the expression of inhibitory receptors like PD-1.

Leishmania major

An intracellular microbe where the outcome of infection depends on the Th1/Th2 balance; Th1 responses eradicate it, while Th2 responses lead the host to succumb to infection.

PD-1

An inhibitory receptor expressed on CD8+ T cells during chronic infections that leads to T cell exhaustion and evades immune elimination.