Study of the T cell receptor repertoire in viral immunodeficiency disease View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1996-12

AUTHORS

Cristina Ciurli, Rafick-Pierre Sékaly, Hugo Soudeyns

ABSTRACT

In recent years, descriptive studies of the T cell repertoire have contributed in several ways to our understanding of immunodeficiency disease. In human AIDS, it was shown that, overall, TCR repertoire perturbations of various magnitude were taking place throughout the course of disease in both the CD4+ and CD8+ T cell subsets. Available evidence suggests that the repertoire is remarkably stable within a given individual in absence of serious pathological conditions, even across long periods of time (Ciurli et al., unpublished). The fact that patients with AIDS present with TCR repertoire perturbations, even throughout the so-called clinically silent phase of the disease, testifies to the extent of immune destruction that is taking place covertly within the peripheral lymphoid tissues. Since preferential deletions of CD4+ T cells expressing specific Vβ subsets are not consistently seen, and since no HIV protein has so far fulfilled all the classical characteristics of SAgs, one must argue that there is so far little support for the proposal that HIV encodes a conventional SAg. Preferential replication of HIV-1 in Vβ12+ cells seemed to provide both specificity and functional purpose for such an HIV-encoded SAg. However, it now seems that this superantigenic activity is in fact associated more closely with CMV infection. The fact that HIV uses SAg activity supplied in trans by a co-infecting pathogen is another good example of how lentiviruses and herpesviruses mutually profit from each other's functions to further their individual replicative needs. Whether this Vβ12 reservoir is in fact pathologically relevant still remains to be addressed.Whereas repertoire studies have failed to reveal the presence of a virally encoded SAg in MAIDS virus infection, they have nevertheless suggested the possibility that indirect, perhaps integration-mediated para-oncogenic events, could be involved in the enhanced expression of endogenousmtv genes, and the observed in vitro Vβ-specific expansions. The importance of indirect SAg expression to the pathogenesis of MAIDS, perhaps in terms of expanding the viral reservoir, is so far unclear.Finally, TCR repertoire studies have also revealed the existence of high-level Vβ-specific expansions, occurring in some patients during the acute phase of HIV infection. All available evidence suggests that these expansions are part of the early cell-mediated immune response to HIV antigens, and are most probably involved in the clearance of the initial viremic episode. These findings are well supported by studies of SIV infection in rhesus macaques. Idiotypic differences in the Vβ expansion patterns, which so far appear to be correlated with disease prognosis, may reflect the differential ability of an individual's TCR repertoire to recognize various HIV cytotoxic epitopes, and/or the relative restriction in the presentation of these peptides by given HLA haplotypes. In other words, a restricted, high-affinity response could be easily counteracted by the virus: selective mutations in cytotoxic epitopes have been documented that abrogate recognition by circulating cytotoxic T cell clones, and that eventually drift far enough from the initial epitope so as to escape presentation by the original class I allele. At the same time, high-level expansion of a T cell clone bearing a high-affinity receptor in the presence of a high viral load could make these T cell clones susceptible to peripheral deletion via high-dose tolerance and clonal exhaustion mechanisms [87]. Several rounds of such a routine would leave the host functionally defenseless with respect to cell-mediated immunity. Through expanded TCR repertoire analysis, we trust that this phenomenon will be revealed in other acute lymphotropic viral infections such as infectious mononucleosis. This type of acute Vβ-specific expansions of T cells expressing activated cytotoxic activity might be a more generalized mechanism of host antiviral response than has been previously thought. More... »

PAGES

319-332

References to SciGraph publications

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/bf01795132

DOI

http://dx.doi.org/10.1007/bf01795132

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1049399872

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/8966659


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25 schema:description In recent years, descriptive studies of the T cell repertoire have contributed in several ways to our understanding of immunodeficiency disease. In human AIDS, it was shown that, overall, TCR repertoire perturbations of various magnitude were taking place throughout the course of disease in both the CD4+ and CD8+ T cell subsets. Available evidence suggests that the repertoire is remarkably stable within a given individual in absence of serious pathological conditions, even across long periods of time (Ciurli et al., unpublished). The fact that patients with AIDS present with TCR repertoire perturbations, even throughout the so-called clinically silent phase of the disease, testifies to the extent of immune destruction that is taking place covertly within the peripheral lymphoid tissues. Since preferential deletions of CD4+ T cells expressing specific Vβ subsets are not consistently seen, and since no HIV protein has so far fulfilled all the classical characteristics of SAgs, one must argue that there is so far little support for the proposal that HIV encodes a conventional SAg. Preferential replication of HIV-1 in Vβ12+ cells seemed to provide both specificity and functional purpose for such an HIV-encoded SAg. However, it now seems that this superantigenic activity is in fact associated more closely with CMV infection. The fact that HIV uses SAg activity supplied in trans by a co-infecting pathogen is another good example of how lentiviruses and herpesviruses mutually profit from each other's functions to further their individual replicative needs. Whether this Vβ12 reservoir is in fact pathologically relevant still remains to be addressed.Whereas repertoire studies have failed to reveal the presence of a virally encoded SAg in MAIDS virus infection, they have nevertheless suggested the possibility that indirect, perhaps integration-mediated para-oncogenic events, could be involved in the enhanced expression of endogenousmtv genes, and the observed in vitro Vβ-specific expansions. The importance of indirect SAg expression to the pathogenesis of MAIDS, perhaps in terms of expanding the viral reservoir, is so far unclear.Finally, TCR repertoire studies have also revealed the existence of high-level Vβ-specific expansions, occurring in some patients during the acute phase of HIV infection. All available evidence suggests that these expansions are part of the early cell-mediated immune response to HIV antigens, and are most probably involved in the clearance of the initial viremic episode. These findings are well supported by studies of SIV infection in rhesus macaques. Idiotypic differences in the Vβ expansion patterns, which so far appear to be correlated with disease prognosis, may reflect the differential ability of an individual's TCR repertoire to recognize various HIV cytotoxic epitopes, and/or the relative restriction in the presentation of these peptides by given HLA haplotypes. In other words, a restricted, high-affinity response could be easily counteracted by the virus: selective mutations in cytotoxic epitopes have been documented that abrogate recognition by circulating cytotoxic T cell clones, and that eventually drift far enough from the initial epitope so as to escape presentation by the original class I allele. At the same time, high-level expansion of a T cell clone bearing a high-affinity receptor in the presence of a high viral load could make these T cell clones susceptible to peripheral deletion via high-dose tolerance and clonal exhaustion mechanisms [87]. Several rounds of such a routine would leave the host functionally defenseless with respect to cell-mediated immunity. Through expanded TCR repertoire analysis, we trust that this phenomenon will be revealed in other acute lymphotropic viral infections such as infectious mononucleosis. This type of acute Vβ-specific expansions of T cells expressing activated cytotoxic activity might be a more generalized mechanism of host antiviral response than has been previously thought.
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32 CD4
33 CD8
34 CMV infection
35 HIV
36 HIV antigen
37 HIV infection
38 HIV proteins
39 HIV-1
40 HLA haplotype
41 MAID
42 SAG expression
43 SAg activity
44 SIV infection
45 T cell clones
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47 T cell repertoire
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49 T cells
50 TCR repertoire
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53 Vβ12
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65 cell subsets
66 cell-mediated immune responses
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69 characteristics
70 class I
71 classical characteristics
72 clearance
73 clones
74 co-infecting pathogens
75 conditions
76 course
77 course of disease
78 cytotoxic activity
79 cytotoxic epitopes
80 deletion
81 descriptive study
82 destruction
83 differences
84 differential ability
85 disease
86 disease prognosis
87 enhanced expression
88 episodes
89 epitopes
90 events
91 evidence
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94 existence
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103 generalized mechanism
104 genes
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106 haplotypes
107 herpesvirus
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112 high-level expansion
113 host
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115 human AIDS
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124 infection
125 infectious mononucleosis
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127 lentivirus
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129 load
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131 lymphoid tissue
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136 mononucleosis
137 mutations
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148 peripheral deletion
149 peripheral lymphoid tissues
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153 place
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155 preferential deletion
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157 presence
158 presentation
159 profit
160 prognosis
161 proposal
162 protein
163 purpose
164 recent years
165 receptor repertoire
166 receptors
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168 relative restriction
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171 repertoire perturbations
172 repertoire studies
173 replication
174 reservoir
175 respect
176 response
177 restriction
178 rhesus macaques
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184 serious pathological conditions
185 silent phase
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191 terms
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193 tissue
194 tolerance
195 trans
196 types
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198 viral infection
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