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. 2013 Dec;37(4):273-83.
doi: 10.1152/advan.00066.2013.

T cell responses: naive to memory and everything in between

Nathan D Pennock  1 , Jason T White, Eric W Cross, Elizabeth E Cheney, Beth A Tamburini, Ross M Kedl
Affiliations

T cell responses: naive to memory and everything in between

Nathan D Pennock et al. Adv Physiol Educ. 2013 Dec.
No abstract available

PubMed Disclaimer

Figures

Fig. 1.
Fig. 1.
T cell activation. A: simplified model of early events in T cell signaling. In the absence of CD28 costimulation, canonical T cell signaling is mostly stalled at the linker for activation of T cells (LAT) signalosome stage, where phospholipase C (PLC)-γ remains unactivated. MHC, major histocompatibility complex; TCR, T cell receptor; P, phosphorylation; ZAP-70, ζ-chain-associated protein kinase 70; IP3, inositol 1,4,5-trisphosphate; PI3K, phosphatidylinositol 3-kinase; B: sustained interaction between a T cell and an antigen-presenting cell (APC) results in the formation of an immunological synapse. Membrane reorganization creates a greater apposition of surface areas into which signaling and adhesion molecules are ordered into a “bulls-eye” arrangement. The relevant molecules are listed according to location. SMAC, supramolecular activation complex; L, ligand; LFA-1, lymphocyte function-associated antigen 1.
Fig. 2.
Fig. 2.
T cell differentiation. Top: APC [i.e., dendritic cell (DC)] recognition of a spectrum of pathogens through various pathogen-associated molecular pattern receptors results in cytokine release from the APC. Along with TCR engagement, milieu cytokines initiate (top middle) differentiation to one of a variety T cell subsets programmed by transcription factors to specifically respond to the spectrum of the instigating pathogen [pathogen and T helper (Th) subset color coordinated]. Upon differentiation, T cells themselves produce cytokines, which feed back into the cellular milieu, amplifying and balancing the immune response to promote specific pathogen clearance (bottom middle) and host survival. Finally, sustained, ill-timed, or otherwise exaggerated T cell immune responses from any of the T cell subsets results in a range of immunopathologies from autoimmunity to allergy and cancer (bottom). IFN, interferon; TGF-β, transforming growth factor-β; Gz, granzyme.
Fig. 3.
Fig. 3.
T cell memory. T cells may assume many phenotypes in response to stimulation. The eventual fate of a T cell depends on many environmental queues, including, but not limited to, cytokines, inflammatory and immune-modulatory products, and tissue-specific factors. These signals, in turn, influence the transcriptional profile of the T cell, leading to developmental choices. Generally, IL-7/15/21 and Eomes/Bcl-6 are considered to tip the scale toward memory. In contrast, IL-2/12, inflammatory products, and T-bet/Blimp-1 weigh toward terminal differentiation and effectors. Exhaustion can result when T cells experience these factors too intensely or for too long. A proper balancing of all these factors will lead to long-lived, protective memory. Markers commonly used to identify cells within a particular functional grouping are given on the right. KLRG-1, killer cell lectin-like receptor subfamily G member 1; PD-1, programmed cell death-1; Lag3, lymphocyte activation gene 3; Tim-3, T cell Ig mucin-3.
Fig. 4.
Fig. 4.
The anatomy of a T cell response. A: microbe invasion and proliferation at the site of infection, leading to the initial recruitment of phagocytes and containment of the infection. Tissue-resident APCs acquire antigen and migrate into the local secondary lymphoid organ (SLO) after being activated by the local inflammatory processes. LN, lymph node. B: during transit, APCs process and present pathogen-derived antigens in the context of class I and class II MHC. APCs also upregulate various cell surface molecules and cytokines important in providing the necessary costimulation to T cells within the SLO. C: antigen-stimulated CD4 T cells collaborate with B cells to promote antibody production, class switching, and memory B cell formation. Both CD4 and CD8 T cells clonally expand and migrate out of the SLO and into the infection site, where their effector functions facilitates the elimination of the pathogen. Aby, antibody; ASC, Antibody secreting cell; D: most T cells die off, leaving a memory pool with precursor frequency, antigen sensitivity, and trafficking capacity optimized for initiating rapid secondary responses in situ. PMN, polymorphonuclear leukocytes.
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