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Chapter 5 : All about T Cells and Induction of Immunity

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Abstract:

In addition to recognizing foreign proteins, T cells also retain a functional memory of virtually all self proteins, which enables them to distinguish between self and nonself antigens. T-cell specificity for antigen and major histocompatibility complex (MHC) is determined by the T-cell receptor (TCR). The TCR is specific for antigen in the form of peptide bound to an MHC protein. Once the TCR binds antigen in association with the appropriate MHC structure, the intracellular segments of the CD3 and ζ chains become phosphorylated as an important early step in T-cell activation. The organization of MHC genes in mice and humans is shown in this chapter. The need for MHC compatibility is explained by the TCR's specificity for self MHC. Vaccines for induction of protective immunity must be designed to induce the appropriate immune response, cell-mediated (Th1) or antibody-mediated (Th2). Humoral antibodies are effective against most bacterial infections; delayed-type hypersensitivity (DTH) is the mechanism of protection against organisms, such as mycobacteria, that infect macrophages; T-cell cytotoxicity is the most effective response to viruses, such as smallpox, that infect epithelial cells. To design a successful vaccine, it is critical to select an immunization strategy that will induce the type of immunity best suited to defend against a specific infection. The current paradigm holds that different types of immune responses can be explained on the basis of two different T-helper cells. T-cell–B-cell collaboration for induction of antibody formation depends on sequential antigen recognition by both cells and an antigen presentation step.

Citation: Sell S. 2001. All about T Cells and Induction of Immunity, p 150-197. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch5
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Figures

Image of Figure 5.2
Figure 5.2

Theoretical growth curve for an antigen-specific T-cell line. Initially rare, these cells increase exponentially through successive rounds of antigen stimulation. In contrast, the nonspecific cells decline over time, due to lack of stimulation. The total cell number declines initially, then increases as antigen-specific T cells become the majority of the population. At this point, cloning by limiting dilution will give a high yield of antigen-specific T cells.

Citation: Sell S. 2001. All about T Cells and Induction of Immunity, p 150-197. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch5
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Image of Figure 5.3
Figure 5.3

Mapping the epitope specificity of a human T-cell line. The response to large recombinant fragments of HBsAG showed specificity for the pre-S1 region. Aseries of synthetic peptides were tested, and three overlapping peptides stimulated the line, mapping the epitope to the 8-amino-acid sequence shared by all three peptides.

Citation: Sell S. 2001. All about T Cells and Induction of Immunity, p 150-197. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch5
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Image of Figure 5.4
Figure 5.4

(A) TCTL cells (CTL) lyse the infected cell before assembly and release of new infectious virus, terminating the infection. (B) Epitope mapping with a series of peptides from influenza nucleoprotein. Target cells were labeled with 51Cr and either infected (A), uninfected (0), or pulsed with nucleoprotein peptides. They were then incubated with influenza-specific TCTL cells from the same donor. Cell lysis was detected as the release of 51Cr from the target cells. (Modified from A. R. M. Townsend, J. Rothbard, F. M. Gotch, G. Bahadur, D. Wraith, and A. J. McMichael, Cell 44:959–968, 1986.)

Citation: Sell S. 2001. All about T Cells and Induction of Immunity, p 150-197. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch5
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Image of Figure 5.5
Figure 5.5

The TCR. Shown is the α- and β-chain heterodimer in association with the γ, α, and ϵ chains of CD3 and the homodimer of the ζ chain. Within the TCR complexes are two copies of the CD3 ϵ chain forming dimers with either γ or δ chains. These chains interact with the enzymatic machinery on the cytoplasmic side of the membrane to generate intracellular activation signals (see below). The TCR chains have cytoplasmic tails of various lengths, which contain immunoreceptor tyrosine-based activation motifs (ITAM) that become phosphorylated at specific sites during T-cell activation through the action of receptor-associated protein tyrosine kinases. These phosphorylations initiate the process of T-cell activation.

Citation: Sell S. 2001. All about T Cells and Induction of Immunity, p 150-197. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch5
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Image of Figure 5.6
Figure 5.6

Combinatorial rearrangement of the variable (V), diversity (D), joining (J), and constant (C) gene segments of the germ line TCR β chain to form two possible TCR genes, one above and one below the germ line gene. The germ line V regions are arranged in tandem. In the process of forming an expressed TCR gene, one of them recombines with a D region, which then recombines with one of the Jβ regions to form a transcriptionally active unit. In general, besides forming a contiguous gene, recombination also brings a promoter upstream of the V region into proximity of an enhancer region located near the C region, causing active transcription of the rearranged gene. Given the 70 V regions times 2 D regions times 6 J regions for each D region, recombination can generate over a thousand distinct TCR α and β chains with different specificities. This number is further greatly increased by junctional diversity, in which new sequences are filled in at the junctions between the V, D, and J regions, in locations that produce new contact residues for antigen binding. Altogether, over 105 combinations of α and β chains are possible, and the product of these (1010) is an upper estimate of the possible number of different receptor specificities.

Citation: Sell S. 2001. All about T Cells and Induction of Immunity, p 150-197. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch5
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Image of Figure 5.7
Figure 5.7

The TCR and activation of CD4+ T cells. At the upper left is depicted the TCR. The sequence of events during T-cell activation upon reaction of the TCR with antigen/MHC complex is as follows. (1) Binding of extracellular domains of α and β chains of Ti to antigen in association with class II MHC. (2) Engagement of CD4/Lck with the TCR and MHC-antigen complex. (3) Activation of Lck proteintyrosine kinase. (4) CD45 stabilizes active Lck. (5) Phosphorylation of ITAMs on γ and ζ chains of TCR. (6) Binding of ZAP-70 SH regions to PO4 on γ and δ chains of TCR and phosphorylation of ZAP-70 by activated Lck. (7) ZAP-70 interacts with LCK SH2 domain to form a stable complex and activate LAT in the cell membrane. (8) LAT recruits the Grb2-Sos complex and PLC to the plasma membrane with phosphorylation and activation of PLCγ1 as well as adaptor proteins Grb2 and Shc, which bind to protein-rich regions in Sos, a guanine nucleotide exchange protein. (9) The Shc-Grb2-Sos complex activates Ras by nucleotide exchange (PKC-independent pathway). (10) PLCγ1, activated by Tec kinase, cleaves phosphatidylinositol 4,5-biphosphate into diglycerol (DG) and inositol phosphate (IP3). (11) IP3 mobilizes intracellular Ca2+ and increases transmembrane flux of extracellular Ca2+. (12) Elevated cytoplasmic Ca2+ activates calcineurin. (13) Calcineurin acts to dephosphorylate and activate nuclear factor of activated T cells (NF-AT). (14) NF-AT relocates to the nucleus, where it binds to DNA and assists in transcriptional activation of the IL-2 gene. (15) Increased PKC activity of membrane DG leads to phosphorylation of a number of cellular proteins and activation of Ras (PKC-dependent pathway). (16) Ras activation leads to a cascade of protein kinase activities culminating in expression of immediate early genes Fos and Jun. (17) Fos/Jun bind to regulatory sequences in DNA along with NF-AT and act to upregulate IL-2 gene expression. (18) IL-2 is secreted and acts as an autocrine factor for stimulating the cell to transit G1 after reaction with the IL-2 receptor (IL-2R). (19) After reaction with IL-2, there is rearrangement of the receptor chains allowing juxtaposition of the Jak kinases (Jak1 with the β chain and Jak3 with the β chain) and phosphorylation of the β chain. (20) One phosphorylation site on the β chain leads to phosphorylation of Shc and activation of Ras. (21) A second dual phosphorylation site further into the cytoplasmic tail of the β chain allows docking of signal transducer and activator of transcription 5 (STAT-5) through its SH2 domain. (22) STAT-5 is phosphorylated, dimerizes, and translocates to the nucleus, where it activates genes for a variety of interleukins and cytokines involved in proliferation of T cells and other cell types. Different STAT molecules may be involved in activation of genes for different cytokines, including but not limited to IL-3, -4, -5, -7, -12, and granulocyte-monocyte colony-stimulating factor as well as IFN-γ. (Modified from A. Weiss, p. 411–447, in W. E. Paul, ed., Fundamental Immunology, 4th ed., Lippincott- Raven, Philadelphia, Pa., 1999.)

Citation: Sell S. 2001. All about T Cells and Induction of Immunity, p 150-197. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch5
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Image of Figure 5.1
Figure 5.1

General scheme of antigen processing and presentation. Exogenous antigen is taken up in endosomes (lower pathway), where it is partially degraded to peptide fragments. Those peptides that bind MHC class II will be transported to the cell surface for presentation to CD4+ T-helper cells. Alternatively, endogenously expressed antigen is processed by cytoplasmic proteases, and the peptide fragments that bind MHC class I are transported to the cell surface and presented to the precursor of CD8+ TCTL cells.

Citation: Sell S. 2001. All about T Cells and Induction of Immunity, p 150-197. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch5
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Image of Figure 5.8
Figure 5.8

Endosomal processing pathway leading to antigen presentation with MHC class II. Class II alpha and beta chains assemble with invariant chain (γ chain) in the ER. They are transported to endosomes, where the invariant chain comes off so peptide can bind. They are then transported to the surface with peptide in the binding groove.

Citation: Sell S. 2001. All about T Cells and Induction of Immunity, p 150-197. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch5
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Image of Figure 5.9
Figure 5.9

Nonendosomal (proteasomal) processing pathway leading to antigen presentation with MHC class I. Class I heavy-chain and β2-microglobulin must wait in the ER until peptide is supplied by the TAP-1/2 peptide transporter. MHC class I needs peptide to form a stable complex that can be transported through the Golgi apparatus and on to the cell surface.

Citation: Sell S. 2001. All about T Cells and Induction of Immunity, p 150-197. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch5
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Image of Figure 5.10
Figure 5.10

Structure of the peptide-binding groove of class II HLA-A2. The black areas at the base of the receptor groove indicate the polymorphic residues of the class II MHC molecule, which are reflected in genetic variations in the ability of different alleles of the class II MHC to present immunogenic peptides. Peptides fit into the groove and interact with the floor and walls. The strength of binding in the groove determines immunogenicity. (Modified from P. J. Bjorkman, M. A. Saper, B. Samraoui, W. S. Bennett, J. L. Strominger, and D. C. Wiley, Nature 329:512–518, 1987.)

Citation: Sell S. 2001. All about T Cells and Induction of Immunity, p 150-197. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch5
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Image of Figure 5.11
Figure 5.11

Genetic maps of the MHC of humans and mice. Three markers, Ke3, Bat I, and Mog, serve to define the relative positions of the other genes in the two species. The human MHC region contains clusters of genes in three designated regions: Mhc class II, Mhc class III, and Mhc class I. The Mhc class II region includes the seven genes encoding the class II MHC molecules, as well as the LMP (processing) and TAP (transporter-associated proteins) involved in antigen processing and presentation. HLA-DR proteins are the major antigen-presenting molecules for exogenous processing and are highly represented on professional APCs, such as memory B cells, macrophages, and tissue resident macrophages. However, they can also be induced on activated T cells and in other tissues when stimulated by inflammatory cytokines such as IFN. The Mhc class III region contains genes for complement components (C4, Bf, and C2) and tumor necrosis factor (TNF-α and -β). The Mhc class I region encodes HLA-A, B, C, E, F, G, and H. HLA-A, B and C are the major class I Mhc antigen-presenting molecules for endogenous antigen processing. The class I antigens are largely responsible for tissue graft rejection and are found on virtually every nucleated cell in the body but are not found on red blood cells. This is why blood transfusions must match for the blood group antigens A, B, and O but not for tissue type, whereas other transplants must match for both or be rejected. Since each person inherits two copies of HLA genes, their tissue type may include up to six different class I alleles. Comparison of the mouse MHC with the human MHC shows that the order of the regions is not the same, with the proximal segment of the mouse region encoding MHC-I. The mouse MHC class I gene H-2K is separated from the other class I genes, H-2D and H-2L, by the MHC-II and MHC-III regions, including the class II genes coding for 1-A and 1-E, and the class III genes for complement components (C2 and C4), enzymes (21-hydroxylase, 21-OH, and glyoxalase [GLO]), and cytokines (TNF). (Modified from D. H. Margulis, p. 263–285, in W. E. Paul, ed., Fundamental Immunology, 4th ed., Lippincott-Raven Publishers, Philadelphia, Pa., 1999.)

Citation: Sell S. 2001. All about T Cells and Induction of Immunity, p 150-197. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch5
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Image of Figure 5.12
Figure 5.12

(A) HLA inheritance within a family, where the probability of a perfect match between two siblings is 0.25. (B) Effect of HLA mismatches on the survival or graft rejection of a transplanted origin.

Citation: Sell S. 2001. All about T Cells and Induction of Immunity, p 150-197. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch5
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Image of Figure 5.13
Figure 5.13

Survival times of kidney allografts among people of different genetic relationships ranging from identical twins to unrelated individuals (cadaver donors). (From W. H. Hildemann, Tissue Antigens 22:1–6, 1983.) Because of better matching and more controlled immunosuppressive regimens, the survival of renal grafts has improved since the time these data were available, but these earlier data show more clearly the effect of tissue matching. At the present time, the 10-year expected survival rates for kidneys from HLA-matched siblings, one haplotype-matched related donors, and cadaver donors are 74, 51, and 40%, respectively. The effects of matching have been largely superseded by controlled immunosuppression.

Citation: Sell S. 2001. All about T Cells and Induction of Immunity, p 150-197. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch5
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Image of Figure 5.14
Figure 5.14

Adoptive transfer of carrier BGG-primed T cells and hapten DNPprimed B cells into an MHC-compatible host. Subsequent immunization with the conjugate DNP-BGG results in antibodies due to T-cell–B-cell collaboration. However, T-cell help requires MHC matching with the B cell (inset).

Citation: Sell S. 2001. All about T Cells and Induction of Immunity, p 150-197. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch5
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Image of Figure 5.15
Figure 5.15

(A) Traditional antigen bridge model of T-cell help. Explains why hapten and carrier must be covalently attached. (B) Antigen presentation model of T-cell help. B cell takes up the antigen via hapten-specific surface immunoglobulin. B cell then processes and presents peptide fragments plus MHC to the T cell.

Citation: Sell S. 2001. All about T Cells and Induction of Immunity, p 150-197. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch5
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Image of Figure 5.16
Figure 5.16

Interactions at the T-cell–B-cell interface. Some are antigen specific, such as TCR binding MHC plus peptide. Others are MHC specific, such as CD4 binding MHC class II. Other interactions are stimulatory, such as CD40L binding CD40 and B7 binding CD28. Finally, some simply help hold the two cells together, such as ICAM-1 and LFA-1 or LFA-3 and CD2.

Citation: Sell S. 2001. All about T Cells and Induction of Immunity, p 150-197. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch5
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Image of Figure 5.17
Figure 5.17

Feedback stimulation between activated T-helper cell expressing CD40L and activated B cell expressing B7. Stimulatory signals flow in both directions, resulting in T-cell production of cytokines. The B cell responds to CD40L plus cytokines by proliferating and by activating class switching. (Modified from E. A. Clark and J. A. Ledbetter, Nature 367:425–428, 1994.)

Citation: Sell S. 2001. All about T Cells and Induction of Immunity, p 150-197. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch5
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Image of Figure 5.18
Figure 5.18

Differential induction of immune response by Th1 and Th2 helper cells. The activities of Th1 and Th2 cells are characterized by the cytokines they produce. Th1 cytokines IL-2, IFN-γ, and TNF-β activate cell-mediated reactions, including immunoglobulin class switching for production of complement-fixing antibodies (opsonins), macrophage activation, and differentiation of CD8 cytotoxic cells. Th2 cytokines IL-3, IL-4, IL-5, and IL-10 are responsible for immunoglobulin class switching for non-complement-fixing antibodies IgG2, IgG4, IgA, and IgE, responsible mainly for mucosal immunity. In addition, IFN-γ secreted by Th1 cells inhibits Th2 effector functions, and IL-4, IL-10, and IL-13 secreted by Th2 cells inhibit Th1 functions. (Modified from A. K. Abbas, K. M. Murphy, and A. Sher, Nature 383:787–793, 1996.)

Citation: Sell S. 2001. All about T Cells and Induction of Immunity, p 150-197. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch5
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Image of Figure 5.19
Figure 5.19

Antibody class switching during primary and secondary immunizations. Priming elicits IgM antibodies of low affinity. During the secondary immunization, B cells receive abundant T-cell help under optimal conditions for class switching from IgM to IgG production and maturation to high-affinity antibodies.

Citation: Sell S. 2001. All about T Cells and Induction of Immunity, p 150-197. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch5
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Image of Figure 5.20
Figure 5.20

Neutralizing sites on influenza virus hemagglutinin are indicated by solid symbols. Residues forming each conformational site share the same symbol. Hemagglutinin structure is based on X-ray crystallography. (Modified from D. C. Wiley, I. A. Wilson, and J. J. Skehel, Nature 289:373–378, 1981.).

Citation: Sell S. 2001. All about T Cells and Induction of Immunity, p 150-197. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch5
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Image of Figure 5.21
Figure 5.21

(A) Incidence of H. influenzae meningitis (in blue) during the first 5 years of life and the corresponding level of anticapsular antibodies (in black). Most disease occurs in the first 2 years of life, after maternal antibodies have waned but before natural exposure has elicited antibodies in the baby. (B) Response to H. influenzae type b (HIB) conjugate vaccine. Unlike the free polysaccharide, the conjugate elicits high-titered anticapsular antibodies at an early age, when protection is needed. (Modified from H. Peltola, H. Kayhty, A. Sivonen, and H. Makela, Pediatrics 60:730–737, 1977, and V. I. Ahonkhai, L. J. Lukacs, L. C. Jonas, H. Matthews, P. P. Vella, R. W. Ellis, J. M. Staub, K. T. Dolan, C. M. Rusk, G. B. Calandra, et al., Pediatrics 85:676–681, 1990.)

Citation: Sell S. 2001. All about T Cells and Induction of Immunity, p 150-197. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch5
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Image of Figure 5.22
Figure 5.22

Diagram depicting the presumptive role of antigen processing and Thelper- cell subsets in different types of immune responses. IgE, IgA, and some IgG subclasses of antibodies result from antigen processing by class II MHC+ dendritic cells that are located in follicles, presentation of antigen to CD4+ T-helper cells, activation of Th2 cells, and differentiation of B cells to produce IgE and IgA. IgG antibodies are produced by B cells if this process involves the Th1 subset of helper cells instead of Th2. DTH also results from activation of Th1 cells, but DTH may result from antigen processing by interdigitating dendritic cells in the T-cell zones of lymph nodes and the action of IL-12. Cytotoxic CD8+ T cells are produced after antigen processing by class I MHC+ cells to CD+ helper cells. DTH cells are CD4+; CTL cells are CD8+. Differentiation of CD8+ cells to TCTL cells is encouraged by IFN-γ and IL-12.

Citation: Sell S. 2001. All about T Cells and Induction of Immunity, p 150-197. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch5
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Image of Figure 5.23
Figure 5.23

Structure of muramyl dipeptide.

Citation: Sell S. 2001. All about T Cells and Induction of Immunity, p 150-197. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch5
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Image of Figure 5.24
Figure 5.24

Cooperative binding of a T-cell epitope with class I MHC and CD8+ TCR. Peptides processed for TCTL-cell recognition have hydrophilic amino acids alternating with hydrophobic amino acids in a manner that aligns the hydrophilic sites on one side of an alpha helix and hydrophobic sites on the other side. The hydrophilic side has affinity for the TCR, whereas the hydrophobic side binds to the class I MHC on the APC. Peptides that have these “amphipathic” structures are presented to reactive CD8+ T cells by the endogenous antigen-processing pathway.

Citation: Sell S. 2001. All about T Cells and Induction of Immunity, p 150-197. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch5
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Image of Figure 5.25
Figure 5.25

Immunostimulating complexes (ISCOMs). ISCOMs form structures with peptide antigens that direct the processing of the antigen to the endogenous pathway, presentation via class I MHC surface molecules, and induction of CD8+ TCTL cells.

Citation: Sell S. 2001. All about T Cells and Induction of Immunity, p 150-197. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch5
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Image of Figure 5.26
Figure 5.26

Recommended childhood immunization schedule (U.S. Public Health Service, January 1999). For details and special recommendations, see http://www.cdc.gov/epo/mmwr/preview.

Citation: Sell S. 2001. All about T Cells and Induction of Immunity, p 150-197. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch5
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Tables

Generic image for table
Table 5.1

Properties of the protein chains of the TCR

Citation: Sell S. 2001. All about T Cells and Induction of Immunity, p 150-197. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch5
Generic image for table
Table 5.2

Chromosomal location of TCR genes in humans and mice

Citation: Sell S. 2001. All about T Cells and Induction of Immunity, p 150-197. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch5
Generic image for table
Table 5.3

T and B-cell activation signals

Citation: Sell S. 2001. All about T Cells and Induction of Immunity, p 150-197. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch5
Generic image for table
Table 5.4

Types of vaccines a

Citation: Sell S. 2001. All about T Cells and Induction of Immunity, p 150-197. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch5
Generic image for table
Table 5.5

Prophylactic immunization for human infectious diseases

Citation: Sell S. 2001. All about T Cells and Induction of Immunity, p 150-197. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch5

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