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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

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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References

    1. Angus KL, Griffiths GM. Cell polarisation and the immunological synapse. Curr Opin Cell Biol 25: 85–91, 2013 - PMC - PubMed
    1. Appleby MW, Gross JA, Cooke MP, Levin SD, Qian X, Perlmutter RM. Defective T cell receptor signaling in mice lacking the thymic isoform of p59fyn. Cell 70: 751–763, 1992 - PubMed
    1. August A, Gibson S, Kawakami Y, Kawakami T, Mills GB, Dupont B. CD28 is associated with and induces the immediate tyrosine phosphorylation and activation of the Tec family kinase ITK/EMT in the human Jurkat leukemic T-cell line. Proc Natl Acad Sci USA 91: 9347–9351, 1994 - PMC - PubMed
    1. Bacchetta R, Passerini L, Gambineri E, Dai M, Allan SE, Perroni L, Dagna-Bricarelli F, Sartirana C, Matthes-Martin S, Lawitschka A, Azzari C, Ziegler SF, Levings MK, Roncarolo MG. Defective regulatory and effector T cell functions in patients with FOXP3 mutations. J Clin Invest 116: 1713–1722, 2006 - PMC - PubMed
    1. Bachmann MF, Wolint P, Walton S, Schwarz K, Oxenius A. Differential role of IL-2R signaling for CD8+ T cell responses in acute and chronic viral infections. Eur J Immunol 37: 1502–1512, 2007 - PubMed