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Chapter 13 : The T-Cell Receptor

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Abstract:

On B cells, specificity is mediated by surface immunoglobulin. On T cells, specificity is mediated by the T-cell receptor (TCR) for antigen. The first indications that T cells recognized antigen through a TCR were derived from functional assays using specific target-cell interactions. The initial identification and isolation of the TCR awaited the development of a panel of monoclonal antibodies (MAbs) that could be used to bind specifically to the TCR. Southern blots were used to find those cDNA molecules that hybridized to a different pattern of restriction-digested DNA when comparing germ line DNA with DNA in the T-cell clones. A transmembrane region, which is characterized by a high level of positively charged amino acids, allows the TCR to be inserted and maintained in the T-cell membrane. Both T cells and B cells express the recombination-activating genes known as and that are responsible for rearrangement of these genes. For the TCR to produce a functional receptor, it must be assembled into the plasma membrane such that it can recognize an appropriate antigen-major histocompatibility complex (MHC) complex displayed to the T cell and must also be able to signal this event to the T cell. Overall, the TCR plays a central role in antigen recognition, and the structural diversity in this molecule represents another example of the use of multiple gene segments to produce a functional molecule with the capacity for recognizing an enormous number of MHC-peptide complexes.

Citation: Ceri H, Mody C. 2004. The T-Cell Receptor, p 297-314. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch13

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Figures

Image of Figure 13.1
Figure 13.1

Killing of virus-infected target cells by T cells is specific for a given virus. Virus-specific T cells are generated by infecting a mouse (strain A) with LCMV and then isolating T lymphocytes from the mouse 2 weeks later. These T cells are then tested for their ability to kill target cells derived from the same mouse strain and infected with either LCMV or a different virus, the mouse mammary tumor virus (MMTV). The T cells from the previously LCMV-infected mouse kill target cells infected with LCMV but do not kill target cells infected with MMTV. Additionally, the immune T cells from strain A mice do not kill strain B cells infected with LCMV, due to production of different MHC proteins by these two different mouse strains.

Citation: Ceri H, Mody C. 2004. The T-Cell Receptor, p 297-314. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch13
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Image of Figure 13.2
Figure 13.2

Illustration of the proposed dual-receptor and altered-self models of T-cell recognition of antigen-MHC. According to the dual-receptor model , antigen and MHC are each recognized by a separate receptor molecule on the T cell. Kappler et al. reasoned that if this model is correct, these two receptors should sort independently on the T-cell surface, such that fusion of two T cells (one recognizing antigen A complexed with MHC A and the other recognizing antigen B complexed with MHC B) would produce a hybrid T cell capable of recognizing any combination of antigen A, antigen B, MHC A, and MHC B. In contrast, the altered-self model holds that one TCR recognizes both antigen and MHC (existing as a complex on the target-cell surface). Kappler et al. reasoned that if this model is correct, the same hybrid T cell would recognize antigen A only in the context of MHC A and would recognize antigen B in the context of MHC B. These studies proved conclusively that the altered-self model is the more accurate model.

Citation: Ceri H, Mody C. 2004. The T-Cell Receptor, p 297-314. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch13
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Image of Figure 13.3
Figure 13.3

Strategy used to clone the gene encoding the TCR, which is based on two assumptions: (i) the gene for the TCR is expressed only in T cells, so mRNA for the TCR can be enriched by subtracting the cDNA prepared by reverse transcription from T-cell mRNA with mRNA isolated from a closely related cell type (in this case, a B cell); and (ii) the gene for the TCR should be randomly rearranged in T-cell clones (to generate unique antigenic specificities) but not in B cells or nonlymphoid cells. After non-T-cell-specific cDNAs are removed by hybridization to B-cell RNA followed by chromatography, the T-cell-specific cDNAs are individually cloned and each used as probes in Southern blots of DNA from liver cells, brain cells, keratinocytes, B cells, and various T-cell clones. cDNA A contains a T-cell-specific transcript that is not rearranged and hence does not represent a TCR cDNA. The same banding pattern is attained for all samples on the blot. However, cDNA B contains a TCR gene, as this DNA is rearranged differently in each T-cell clone examined, giving a unique banding pattern for each T-cell clone. Hybridization of one cDNA clone with DNA from multiple T-cell clones is based on the annealing of the constant region genes that are conserved within each different class of TCR chain.

Citation: Ceri H, Mody C. 2004. The T-Cell Receptor, p 297-314. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch13
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Image of Figure 13.4
Figure 13.4

The structure of the TCR is similar to that of immunoglobulin (stippled box around one immunoglobulin Fab fragment highlights the region of strongest structural similarity). Like an immunoglobulin, the TCR is composed of two types of protein chains (α and β chains), each consisting of a tandem array of immunoglobulin- like domains. Each protein chain is a different color, and each immunoglobulin- like domain is represented by a shaded circle. In addition, the arrangement of disulfide bonds (-s-s-) is similar in TCR and immunoglobulin, with each immunoglobulin-like domain containing one intradomain disulfide bond and each protein chain attached to the others by interchain disulfide bonds. In each case, the antigen-binding site exists at the interface of two protein chains and is located at the most membrane-distal end of the protein.

Citation: Ceri H, Mody C. 2004. The T-Cell Receptor, p 297-314. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch13
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Image of Figure 13.5
Figure 13.5

A side-by-side comparison of backbone carbon tracings of the TCR and an antibody Fab fragment . TRAJ (J) and IGLJ (J) are depicted in yellow, TRBJ (J) and IGHJ (J) are depicted in cyan, and TRBD (D) and IGHD (D) are shown in red. Green regions indicate areas where nontemplated nucleotides (N-nucleotides) were inserted during V(D)J recombination. Modified from I. A. Wilson and K. C. Garcia, 839–848, 1997, with permission.

Citation: Ceri H, Mody C. 2004. The T-Cell Receptor, p 297-314. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch13
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Image of Figure 13.6
Figure 13.6

Backbone carbon tracings of two TCRs complexed with peptide-MHC. CDRs of the TCRs are color coded as follows: CDR1α (blue), CDR2α (purple), CDR3α (green), CDR1β (cyan), CDR2β (pink), CDR3β (yellow), and HV4 (orange). Reprinted from I. A. Wilson and K. C. Garcia, 839–848, 1997, with permission.

Citation: Ceri H, Mody C. 2004. The T-Cell Receptor, p 297-314. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch13
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Image of Figure 13.7
Figure 13.7

Germ line organization of the human TCRα (TRA) and TCR δ (TRD) gene families. Functional V genes for both the TRAV and TRDV polypeptides are shown in green, and pseudogenes are shown in red. Variable-region genes with single numbers are not part of a subgroup. Variable-region genes with a hyphenated number (i.e., 13-1) indicate the subgroup (first number) and gene within that subgroup (second number). Genes with a composite designation including a forward slash (/) and a DV number can be incorporated into variable regions of either TCR α or TCR δ chains. Variableregion genes exclusively used in TCR δ chains are designated TRDV. Note TRDV3 is 3ʹ of the TRDC gene and transcribed in the opposite direction (arrow). Solid yellow bars represent functional joining-region genes, red bars are pseudogenes, and pink bars indicate potential open reading frames for which no protein has yet been found. TCR δ-chain diversity- region genes are in dark blue (TRDD1 to 3). Constant-region genes are in light blue (TRDC and TRAC). Enhancers (cyan) refer to regulatory genetic elements that promote transcription of the genes in this region. From IMGT (http//imgt.cines.fr) with permission from M.-P. Lefranc.

Citation: Ceri H, Mody C. 2004. The T-Cell Receptor, p 297-314. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch13
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Image of Figure 13.8
Figure 13.8

Germ line organization of the human TCRβ (TRB) gene locus. Boxes are not to scale and exons are not indicated. Functional V genes for the TRBV polypeptides are shown in green, pseudogenes are in red, and yellow boxes indicate potential open reading frames for which no protein has yet been found. Variableregion genes with single numbers are not part of a subgroup. Variable-region genes with a hyphenated number (i.e., 3-1) indicate the subgroup (first number) and gene within that subgroup (second number). Darker yellow bars represent two joining-region gene clusters with six or seven genes (J1-1 to J1-6 and J2-1 to J2-7). TCR β-chain diversity-region genes are in light purple (TRBD1 and TRBD2). Constant-region genes are in blue (TRBC1 and C2). Enhancer (cyan) refers to regulatory genetic elements that promote transcription of the genes in this region. Purple boxes (filled, functional; empty, pseudogenes) represent genes not related to TCR production. From IMGT (http://imgt.cines.fr) with permission from M.-P. Lefranc.

Citation: Ceri H, Mody C. 2004. The T-Cell Receptor, p 297-314. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch13
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Image of Figure 13.9
Figure 13.9

Germ line organization of the human TCRγ (TRG) gene locus. Boxes are not to scale and exons are not indicated. A double arrow indicates an insertion or deletion polymorphism. Functional V genes for the TRGV polypeptides are shown in green, pseudogenes are in red, and yellow boxes indicate potential open reading frames for which no protein has yet been found. All TRGV genes that are not pseudogenes are designated by a number. Two clusters represent the TRGJ (orange-yellow) and TRGC (blue) regions. Enhancer (cyan) refers to regulatory genetic elements that promote transcription of the genes in this region. Silencer (yellow circle) refers to a regulatory genetic element that inhibits transcription from the region. From IMGT (http://imgt.cines.fr) with permission from M.-P. Lefranc.

Citation: Ceri H, Mody C. 2004. The T-Cell Receptor, p 297-314. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch13
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Image of Figure 13.10
Figure 13.10

Germ line organization of the mouse TCRα (TRA) and TCRδ (TRD) gene families. The boxes representing the genes are not to scale. Exons are not shown. Variable-region genes for TRAV and TRDV are designated by a number for the subgroup followed, whenever there are several genes belonging to the same subgroup, by a hyphen and a number for their relative localization. Numbers increase from 5ʹ to 3ʹ in the locus. Functional V genes for the TRAV polypeptides are shown in green, pseudogenes are in red, and solid yellow boxes indicate potential open reading frames for which no protein has yet been found. The solid blue line and the dashed blue line below the map represent two parts of the locus that are duplicated. The TRAV genes of the proximal V cluster (closer to the telomere) are designated by a number for the subgroup, followed by a hyphen and a number for the localization from 3ʹ to 5ʹ in the locus. The TRAV genes of the distal duplicated V cluster (closer to the centromere) are designated by the same numbers as the corresponding genes in the proximal V cluster, with the letter D added. Single arrows show two genes, TRAV7-2 and TRDV5, whose transcriptional polarity is opposite to that of the TRA JC cluster and the TRD DJC cluster. TRDD-region genes are in dark blue, functional joining-region genes in orange-yellow, pseudogenes in red; and joining-region pink boxes indicate potential open reading frames for which no protein has yet been found. Constant-region genes are in lighter blue. From IMGT (http://imgt.cines.fr) with permission from M.-P. Lefranc.

Citation: Ceri H, Mody C. 2004. The T-Cell Receptor, p 297-314. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch13
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Image of Figure 13.11
Figure 13.11

Germ line organization of the mouse TCRβ (TRB) gene locus. Boxes are not to scale and exons are not indicated. A single arrow shows the most 3ʹ TRBV gene whose transcriptional polarity is opposite to that of the DJC cluster. Functional V genes for the TRBV polypeptides are shown in green, pseudogenes are in red, and yellow boxes indicate potential open reading frames for which no protein has yet been found. Variable- region genes with single numbers are not part of a subgroup. Variable-region genes with a hyphenated number (i.e., 3-1) indicate the subgroup (first number) and gene within that subgroup (second number). Orange- yellow bars represent two joining-region gene clusters with six or seven genes (J1-1 to J1-6 and J2-1 to J2-7). TCR β-chain diversity-region genes are in dark blue (TRBD1 and TRBD2). Constant-region genes are in a lighter blue (TRBC1 and C2). From IMGT (http://imgt.cines.fr) with permission from M.-P. Lefranc.

Citation: Ceri H, Mody C. 2004. The T-Cell Receptor, p 297-314. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch13
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Image of Figure 13.12
Figure 13.12

Germ line organization of the mouse TCRγ (TRG) gene locus. Boxes are not to scale and exons are not indicated. Horizontal arrows show genes whose polarity is opposite to that of the locus. Functional V genes for the TRGV polypeptides are shown in green and yellow boxes indicate potential open reading frames for which no protein has yet been found. All mouse TRGV genes are designated by a number. Four clusters represent the TRGJ (orange-yellow) and TRGC (blue) regions. The mouse TRGJ3/C3 cluster is not expressed. Enhancer (cyan) refers to regulatory genetic elements that promote transcription of the genes in this region. From IMGT (http://imgt.cines.fr) with permission from M.-P. Lefranc.

Citation: Ceri H, Mody C. 2004. The T-Cell Receptor, p 297-314. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch13
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Image of Figure 13.13
Figure 13.13

Comparison of RSS arrangement in immunoglobulin (Ig) versus that in TCR. Similar to Ig, V, D, and J segments of the TCR chain loci are flanked by 12-bp and 23-bp RSSs. However, the arrangement of these RSSs differs between TCR and Ig. Most notable is the difference in RSS arrangement flanking the D segments. In the Ig heavy-chain locus, the same type of RSS is found upstream and downstream of each D segment, which prevents D segments from joining to each other. In the TCR β- and δ-chain loci, each D segment is flanked upstream by a 12-bp RSS and downstream by a 23-bp RSS. () The arrangement of RSSs in the TCR β- and δ-chain loci allows joining of multiple D segments in one rearranged variable-domain exon, while still obeying the 12/23 rule.

Citation: Ceri H, Mody C. 2004. The T-Cell Receptor, p 297-314. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch13
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Image of Figure 13.14
Figure 13.14

Schematic diagram comparing variability within a TCR variable domain versus that within an immunoglobulin domain. For clarity, the TCR curve (pink) is in the foreground on the left side, while the immunoglobulin curve (yellow) is in the foreground on the right side. Bars at the top indicate the extent of the CDRs. The chart below the graph indicates the extent to which various molecular mechanisms contribute to variability in each CDR of the V region.

Citation: Ceri H, Mody C. 2004. The T-Cell Receptor, p 297-314. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch13
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Image of Figure 13.15
Figure 13.15

Overall structure of a γδ TCR, αβ TCR, and Fabs. γδ TCR (red); αβ TCR (green); () three Fabs (blue) showing the angle between the V and C domains. The V domains are at the top of each depiction. The γδ TCR V regions have a smaller angle between them when compared with the other antigen-binding molecules, and the γδ C regions are more separated from each other than the αβ TCR C regions or HL Fab C regions. The δ, β, and H chains are the lighter shades, and the γ, α, and L chains are the darker shades. Reprinted from T. J. Allison et al., 820–824, 2001, with permission from D. Garboczi and (Macmillan Publishers Ltd.).

Citation: Ceri H, Mody C. 2004. The T-Cell Receptor, p 297-314. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch13
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Image of Figure 13.16
Figure 13.16

The CD3 complex consists of six polypeptide chains in association with two (or more) TCRs. The CD3 complex depicted contains a homodimer of ζ chains; however, some CD3 complexes contain a ζη heterodimer instead of a ζζ homodimer (not shown). The ζ and η chains have three ITAMs per chain, while the γ, δ, and ε chains have a single ITAM per chain. The ITAMs interact with the Fyn and ZAP-70 protein tyrosine kinase.

Citation: Ceri H, Mody C. 2004. The T-Cell Receptor, p 297-314. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch13
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Image of Figure 13.17
Figure 13.17

Association of the protein kinases Lck, Fyn, and ZAP- 70 with components of CD3 results in tyrosine phosphorylation that transmits the signal for cellular activation. The following are the steps of signal transduction: the tyrosine phosphatase CD45 removes an inhibitory phosphate group from the Src family kinase Fyn, thus activating Fyn; CD45 likewise removes an inhibitory phosphate group from the Lck kinase, activating Lck; active Fyn phosphorylates multiple ITAMs on the cytoplasmic tails of the proteins of the CD3 complex; phosphorylated ITAMs of CD3 ζ chain form a docking site that recruits the ZAP-70 kinase to CD3; (hatched arrow) active Lck phosphorylates and thus activates CD3-bound ZAP-70; (not shown) active ZAP-70 phosphorylates and activates phospholipase Cγ1 (PLCγ1). Active PLCγ1 can then mediate downstream signaling events. Dots indicate phosphorylation. Adapted from M. Izquierdo and D. A. Cantrell, 268–271, 1992.

Citation: Ceri H, Mody C. 2004. The T-Cell Receptor, p 297-314. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch13
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Image of Figure 13.18
Figure 13.18

The CD4 and CD8 accessory molecules. The CD4 molecule binds to the β domain of MHC class II. The CD8 accessory molecule binds to the α and α domains of MHC class I. The stereo view of the structure of a CD8 αα homodimer with HLA-A2 MHC and cognate peptide showing the interaction surfaces of the complex. The HLA-A2 heavy chain (green), β microglobulin (gold), CD8α subunit 1 (red), and CD8α subunit 2 (blue) are depicted schematically, and the peptide bound to the MHC is shown in white as a ball-and-stick representation. The CD8 α chain contains two immunoglobulin- like folds (red and blue), and the loops (thin part of ribbon structure) of the domains, analogous to the CDR loops of variable regions, come in contact with the MHC molecule. The two subunits do not have an equal contribution to the binding to MHC class I. Both subunits make interactions through all of their CDR-like loops with the α 3 domain. However, the first subunit domain contacts both the α2 and α3 portions of MHC class I. Reprinted from G. F. Gao et al., 630–634, 1997, with permission from E. Y. Jones and (Macmillan Publishers Ltd.).

Citation: Ceri H, Mody C. 2004. The T-Cell Receptor, p 297-314. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch13
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Image of Figure 13.19
Figure 13.19

Accessory molecules involved in T-cell binding to an APC. In addition to the MHC-antigen binding to the TCR, other receptor-ligand pairs increase the affinity of binding between a T cell and an APC and can also contribute to signal transduction in T-cell activation. Although CD80 and CD86 both interact with CD28 and CTLA-4, CD80 tends to interact preferentially with CTLA-4 and CD86 tends to interact with CD28.

Citation: Ceri H, Mody C. 2004. The T-Cell Receptor, p 297-314. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch13
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References

/content/book/10.1128/9781555816148.chap13
1. Allison, T. J.,, and D. N. Garboczi. 2002. Structure of gamma/delta T cell receptors and their recognition of non-peptide antigens. Mol. Immunol. 38:10511061.
2. Carding, S. R.,, and P. J. Egan. 2002. Gamma/delta T cells: functional plasticity and heterogeneity. Nat. Rev. Immunol. 2:336345.
3. Davis, M. M.,, J. J. Boniface,, Z. Reich,, D. L. Lyons,, J. Hampl,, B. Arden,, and Y.-H. Chien. 1998. Ligand recognition by T cell receptors. Annu. Rev. Immunol. 16:523544.
4. Khor, B.,, and B. P. Sleckman. 2002. Allelic exclusion at the TCRbeta locus. Curr. Opin. Immunol. 14:230234.
5. LeFranc, M. P.,, and G. LeFranc. 2001. The T Cell Receptor Facts Book. Academic Press, New York, N.Y..
6. Lord, G. M.,, R. I. Lechler,, and A. J. T. George. 1999. A kinetic differentiation model for the action of altered TCR ligands. Immunol. Today 20:3339.
7. Rudolph, M. G.,, and I. A. Wilson. 2002. The specificity of TCR/pMHC interaction. Curr. Opin. Immunol. 14:5265.
8. Rubin, B.,, L. Alibaud,, A. Huchenq-Champagne,, J. Arnaud,, M. L. Toribio,, and J. Constans. 2002. Some hints concerning the shape of T-cell receptor structures. Scand. J. Immunol. 55:111118.
9. Wang, J. H.,, and E. L. Reinherz. 2002. Structural basis of T cell recognition of peptides bound to MHC molecules. Mol. Immunol. 38:10391049.

Tables

Generic image for table
Table 13.1

Comparison of the number of V, D, and J genes in the germ line of human immunoglobulin (Ig) and TCR genes

Citation: Ceri H, Mody C. 2004. The T-Cell Receptor, p 297-314. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch13

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