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Academic literature on the topic 'Antigen receptor sharing'
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Journal articles on the topic "Antigen receptor sharing"
1
Thomas, Paul Glyndwr, Pradyot Dash, Tomer Hertz, Andrew Gartland, and Philip Bradley. "High rates of cross-reactivity among apparently unrelated specificities shape antigen-specific T cell receptor repertoires." Journal of Immunology 196, no. 1_Supplement (2016): 133.30. http://dx.doi.org/10.4049/jimmunol.196.supp.133.30.
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Abstract We have analyzed several thousand antigen-specific T cell receptor repertoires from multiple animals infected with influenza virus and/or murine cytomegalovirus (mCMV). Insights into the overall structure of antigen-specific repertoire landscapes towards 7 different specificities were generated from single cell paired TCR αβ sequencing. In addition to characterization of repertoire features such as diversity, clonal structure, convergent recombination, and key deterministic features of antigen-specificity, we observed a surprisingly high rate of single or dual chain sharing between otherwise unrelated responses. These shared receptors were often observed across multiple animals in independent experiments. However, sharing appeared more likely to occur in animals where the two epitopes were presented simultaneously. Cloning and expression of these unique specificities has allowed further receptor characterization. Additional data indicate that some combinations of co-presented epitopes result in broader repertoires recruited to one or both epitopes. In summary, T cell receptors have a significant propensity for cross-reactivity across otherwise unrelated specificities, an effect that appears to be driven by co-presentation and substantially shapes the magnitude and diversity of antigen-specific repertoires.
2
Johnson, Sarah, Rachel M. Gittelman, Catherine Sanders, and Harlan Robins. "Determining the impact of HLA type and chronic viral infection on peripheral T-cell receptor sharing between unrelated individuals." Journal of Immunology 204, no. 1_Supplement (2020): 140.16. http://dx.doi.org/10.4049/jimmunol.204.supp.140.16.
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Abstract T cells generate highly diverse T-cell receptors (TCRs) to recognize antigens, most of which are private to each individual. TCRs with low junctional complexity have a higher likelihood of being generated and shared across individuals. Additional factors that may further limit diversity and increase the likelihood that particular TCRs are public include: (a) thymus selection for maturation of TCRs that bind antigens presented by an individual’s human leukocyte antigen (HLA) proteins, and (b) T-cell proliferation upon exposure to cognate antigens, which remain in the periphery as memory T cells. Numerous public TCRs have been associated with particular HLA restrictions and antigen specificities1. Chowell et al. also showed that HLA diversity is important for mounting an effective T-cell response against solid tumors2. However, little is known about the impact of these forces on the diversity of the TCR repertoire and expected TCR sharing across individuals. Here, we leverage the TCR repertoires of 666 healthy individuals sequenced with the immunoSEQ® Assay (Adaptive Biotechnologies, Seattle, WA) to address these questions. We investigate (a) how HLA restriction affects immune repertoires by examining the effect of HLA heterozygosity and divergence on the diversity of the TCR repertoire; (b) how the similarity of HLA alleles between individuals impacts the number of TCRs shared between individuals and (c) the impact of shared antigen exposure by determining how age and CMV status impacts clone sharing between individuals. These data show that HLA type, age, and CMV exposure shape the immune repertoire and influence the sharing of clones between individuals.
3
Johnson, Sarah A., Spencer L. Seale, Rachel M. Gittelman, Julie A. Rytlewski, Harlan S. Robins, and Paul A. Fields. "Impact of HLA type, age and chronic viral infection on peripheral T-cell receptor sharing between unrelated individuals." PLOS ONE 16, no. 8 (2021): e0249484. http://dx.doi.org/10.1371/journal.pone.0249484.
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The human adaptive immune system must generate extraordinary diversity to be able to respond to all possible pathogens. The T-cell repertoire derives this high diversity through somatic recombination of the T-cell receptor (TCR) locus, a random process that results in repertoires that are largely private to each individual. However, factors such as thymic selection and T-cell proliferation upon antigen exposure can affect TCR sharing among individuals. By immunosequencing the TCRβ variable region of 426 healthy individuals, we find that, on average, fewer than 1% of TCRβ clones are shared between individuals, consistent with largely private TCRβ repertoires. However, we detect a significant correlation between increased HLA allele sharing and increased number of shared TCRβ clones, with each additional shared HLA allele contributing to an increase in ~0.01% of the total shared TCRβ clones, supporting a key role for HLA type in shaping the immune repertoire. Surprisingly, we find that shared antigen exposure to CMV leads to fewer shared TCRβ clones, even after controlling for HLA, indicative of a largely private response to major viral antigenic exposure. Consistent with this hypothesis, we find that increased age is correlated with decreased overall TCRβ clone sharing, indicating that the pattern of private TCRβ clonal expansion is a general feature of the T-cell response to other infectious antigens as well. However, increased age also correlates with increased sharing among the lowest frequency clones, consistent with decreased repertoire diversity in older individuals. Together, all of these factors contribute to shaping the TCRβ repertoire, and understanding their interplay has important implications for the use of T cells for therapeutics and diagnostics.
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Ritvo, Paul-Gydeon, Ahmed Saadawi, Pierre Barennes, et al. "High-resolution repertoire analysis reveals a major bystander activation of Tfh and Tfr cells." Proceedings of the National Academy of Sciences 115, no. 38 (2018): 9604–9. http://dx.doi.org/10.1073/pnas.1808594115.
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T follicular helper (Tfh) and regulatory (Tfr) cells are terminally differentiated cells found in germinal centers (GCs), specialized secondary lymphoid organ structures dedicated to antibody production. As such, follicular T (Tfol) cells are supposed to be specific for immunizing antigens, which has been reported for Tfh cells but is debated for Tfr cells. Here, we used high-throughput T cell receptor (TCR) sequencing to analyze the repertoires of Tfh and Tfr cells, at homeostasis and after immunization with self- or foreign antigens. We observed that, whatever the conditions, Tfh and Tfr cell repertoires are less diverse than those of effector T cells and Treg cells of the same tissues; surprisingly, these repertoires still represent thousands of different sequences, even after immunization with a single antigen that induces a 10-fold increase in Tfol cell numbers. Thorough analysis of the sharing and network of TCR sequences revealed that a specific response to the immunizing antigen can only, but hardly, be detected in Tfh cells immunized with a foreign antigen and Tfr cells immunized with a self-antigen. These antigen-specific responses are obscured by a global stimulation of Tfh and Tfr cells that appears to be antigen-independent. Altogether, our results suggest a major bystander Tfol cell activation during the immune response in the GCs.
5
Messmer, Bradley T., Emilia Albesiano, Dimitar G. Efremov, et al. "Multiple Distinct Sets of Stereotyped Antigen Receptors Indicate a Role for Antigen in Promoting Chronic Lymphocytic Leukemia." Journal of Experimental Medicine 200, no. 4 (2004): 519–25. http://dx.doi.org/10.1084/jem.20040544.
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Previous studies suggest that the diversity of the expressed variable (V) region repertoire of the immunoglobulin (Ig)H chain of B-CLL cells is restricted. Although limited examples of marked constraint in the primary structure of the H and L chain V regions exist, the possibility that this level of restriction is a general principle in this disease has not been accepted. This report describes five sets of patients, mostly with unmutated or minimally mutated IgV genes, with strikingly similar B cell antigen receptors (BCRs) arising from the use of common H and L chain V region gene segments that share CDR3 structural features such as length, amino acid composition, and unique amino acid residues at recombination junctions. Thus, a much more striking degree of structural restriction of the entire BCR and a much higher frequency of receptor sharing exists among patients than appreciated previously. The data imply that either a significant fraction of B-CLL cells was selected by a limited set of antigenic epitopes at some point in their development and/or that they derive from a distinct B cell subpopulation with limited Ig V region diversity. These shared, stereotyped Ig molecules may be valuable probes for antigen identification and important targets for cross-reactive idiotypic therapy.
6
Sherman, D. H., P. S. Hochman, R. Dick, et al. "Molecular analysis of antigen recognition by insulin-specific T-cell hybridomas from B6 wild-type and bm12 mutant mice." Molecular and Cellular Biology 7, no. 5 (1987): 1865–72. http://dx.doi.org/10.1128/mcb.7.5.1865-1872.1987.
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Molecular analysis of the heterodimeric T-cell antigen receptor of insulin-specific class II-restricted T-cell hybridomas (THys) derived from C57BL/6 (B6) wild-type and B6.C-H-2bm12 (bm12) mutant mice revealed that such T cells use a diverse V gene repertoire. Analysis of three THys that use related V genes, however, showed a number of novel features. Two THys that share major histocompatibility complex restriction use V alpha genes that are 98.6% homologous. Two THys sharing the same antigen fine specificity use a particular germ line V beta D beta J beta combination. A 21-base-pair deletion in the 5' segment of the J beta gene occurs in one THy, suggesting a novel mechanism for generating diversity in T-cell antigen receptor beta genes. The first amino acid encoded by N sequences at the V-D junction is conserved in a pair of T cells which recognize identical antigenic epitopes. The implications of these findings for the structural mechanisms underlying major histocompatibility complex-restricted antigen-specific T-cell recognition are discussed.
7
Sherman, D. H., P. S. Hochman, R. Dick, et al. "Molecular analysis of antigen recognition by insulin-specific T-cell hybridomas from B6 wild-type and bm12 mutant mice." Molecular and Cellular Biology 7, no. 5 (1987): 1865–72. http://dx.doi.org/10.1128/mcb.7.5.1865.
Full textAbstract:
Molecular analysis of the heterodimeric T-cell antigen receptor of insulin-specific class II-restricted T-cell hybridomas (THys) derived from C57BL/6 (B6) wild-type and B6.C-H-2bm12 (bm12) mutant mice revealed that such T cells use a diverse V gene repertoire. Analysis of three THys that use related V genes, however, showed a number of novel features. Two THys that share major histocompatibility complex restriction use V alpha genes that are 98.6% homologous. Two THys sharing the same antigen fine specificity use a particular germ line V beta D beta J beta combination. A 21-base-pair deletion in the 5' segment of the J beta gene occurs in one THy, suggesting a novel mechanism for generating diversity in T-cell antigen receptor beta genes. The first amino acid encoded by N sequences at the V-D junction is conserved in a pair of T cells which recognize identical antigenic epitopes. The implications of these findings for the structural mechanisms underlying major histocompatibility complex-restricted antigen-specific T-cell recognition are discussed.
8
Silins, S. L., S. M. Cross, S. L. Elliott, et al. "Development of Epstein-Barr virus-specific memory T cell receptor clonotypes in acute infectious mononucleosis." Journal of Experimental Medicine 184, no. 5 (1996): 1815–24. http://dx.doi.org/10.1084/jem.184.5.1815.
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The importance of cytotoxic T lymphocytes (CTLs) in the immunosurveillance of Epstein-Barr virus (EBV)-infected B cells is firmly established, and the viral antigens of CTL recognition in latent infection are well defined. The epitopes targeted by CTLs during primary infection have not been identified, however, and there is only limited information about T cell receptor (TCR) selection. In the present report, we have monitored the development of memory TCR-beta clonotypes selected in response to natural EBV infection in a longitudinal study of an HLA-B8+ individual with acute infectious mononucleosis (IM). By stimulating peripheral blood lymphocytes with HLA-B8+ EBV-transformed B lymphoblastoid cells, the primary virus-specific CTL response was shown to include specificities for two HLA-B8-restricted antigenic determinants, FLRGRAYGL and QAKWRLQTL, which are encoded within the latent EBV nuclear antigen EBNA-3. TCR-beta sequence analysis of CTL clones specific for each epitope showed polyclonal TCR-beta repertoire selection, with structural restrictions on recognition that indicated antigen-driven selection. Furthermore, longitudinal repertoire analysis revealed long-term preservation of a multiclonal effector response throughout convalescence, with the reemergence of distinct memory T cell clonotypes sharing similar structural restrictions. Tracking the progression of specific TCR-beta clonotypes and antigen-specific TCR-V beta family gene expression in the peripheral repertoire ex vivo using semiquantitative PCR strongly suggested that selective TCR-beta expansions were present at the clonotype level, but not at the TCR-V beta family level. Overall, in this first analysis of antigen-specific TCR development in IM, a picture of polyclonal TCR stimulation is apparent. This diversity may be especially important in the establishment of an effective CTL control during acute EBV infection and in recovery from disease.
9
Qi, Qian, Mary M. Cavanagh, Sabine Le Saux, et al. "Diversification of the antigen-specific T cell receptor repertoire after varicella zoster vaccination." Science Translational Medicine 8, no. 332 (2016): 332ra46. http://dx.doi.org/10.1126/scitranslmed.aaf1725.
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Diversity and size of the antigen-specific T cell receptor (TCR) repertoire are two critical determinants for successful control of chronic infection. Varicella zoster virus (VZV) that establishes latency during childhood can escape control mechanisms, in particular with increasing age. We examined the TCR diversity of VZV-reactive CD4 T cells in individuals older than 50 years by studying three identical twin pairs and three unrelated individuals before and after vaccination with live attenuated VZV. Although all individuals had a small number of dominant T cell clones, the breadth of the VZV-specific repertoire differed markedly. A genetic influence was seen for the sharing of individual TCR sequences from antigen-reactive cells but not for repertoire richness or the selection of dominant clones. VZV vaccination favored the expansion of infrequent VZV antigen–reactive TCRs, including those from naïve T cells with lesser boosting of dominant T cell clones. Thus, vaccination does not reinforce the in vivo selection that occurred during chronic infection but leads to a diversification of the VZV-reactive T cell repertoire. However, a single-booster immunization seems insufficient to establish new clonal dominance. Our results suggest that repertoire analysis of antigen-specific TCRs can be an important readout to assess whether a vaccination was able to generate memory cells in clonal sizes that are necessary for immune protection.
10
Cosmi, Lorenzo, Francesco Liotta, Elena Lazzeri, et al. "Human CD8+CD25+ thymocytes share phenotypic and functional features with CD4+CD25+ regulatory thymocytes." Blood 102, no. 12 (2003): 4107–14. http://dx.doi.org/10.1182/blood-2003-04-1320.
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Abstract CD8+CD25+ cells, which expressed high levels of Foxp3, glucocorticoid-induced tumor necrosis factor receptor (GITR), CCR8, tumor necrosis factor receptor 2 (TNFR2), and cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) mRNAs, were identified in the fibrous septa and medullary areas of human thymus. Activated CD8+CD25+ thymocytes did not produce cytokines, but most of them expressed surface CTLA-4 and transforming growth factor β1 (TGF-β1). Like CD4+CD25+, CD8+CD25+ thymocytes suppressed the proliferation of autologous CD25-T cells via a contact-dependent mechanism. The suppressive activity of CD8+CD25+ thymocytes was abrogated by a mixture of anti-CTLA-4 and anti-TGF-β1 antibodies and it was mediated by their ability to inhibit the expression of the interleukin 2 receptor α chain on target T cells. These results demonstrate the existence of a subset of human CD8+CD25+ thymocytes sharing phenotype, functional features, and mechanism of action with CD4+CD25+ T regulatory cells. (Blood. 2003;102:4107-4114)