Identification of effector-memory CMV-specific T lymphocytes that kill CMV-infected target cells in an HLA-E-restricted fashion

Mazzarino, Paola; Pietra, Gabriella; Vacca, Paola; Falco, Michela; Colau, Didier; Coulie, Pierre G.; Moretta, Alessandro; Mingari, Maria Cristina

doi:10.1002/eji.200535343

Cited by 75 publications

(86 citation statements)

References 44 publications

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“…This is in line with the observation that the use of short, generally 9mer, peptides is unlikely to elicit HLA class IIrestricted T cell responses [39,46], and the fact that most of the tested subjects were chronically HIV infected with a low prevalence of detectable CD4 T cell responses [17]. Similarly, while recent studies report a role for HLA-E in the presentation of viral [47,48] and bacterial [49,50] peptides to CD8 T cells, it is unlikely that the observed reactivities were due to common epitope presentation on HLA-E alleles, given the near-monomorphic nature of HLA-E that would dominate the statistical analyses that identify alleles in more diverse loci [49].…”

Section: Discussionsupporting

confidence: 85%

Extensive HLA class I allele promiscuity among viral CTL epitopes

et al. 2007

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Promiscuous binding of T helper epitopes to MHC class II molecules has been well established, but few examples of promiscuous class I-restricted epitopes exist. To address the extent of promiscuity of HLA class I peptides, responses to 242 well-defined viral epitopes were tested in 100 subjects regardless of the individuals' HLA type. Surprisingly, half of all detected responses were seen in the absence of the originally reported restricting HLA class I allele, and only 3% of epitopes were recognized exclusively in the presence of their original allele. Functional assays confirmed the frequent recognition of HLA class I-restricted T cell epitopes on several alternative alleles across HLA class I supertypes and encoded on different class I loci. These data have significant implications for the understanding of MHC class I-restricted antigen presentation and vaccine development.

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Section: Discussionsupporting

confidence: 85%

Extensive HLA class I allele promiscuity among viral CTL epitopes

et al. 2007

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“…These molecules are also recognized by αβTCR-bearing T cells and are important in fending off infectious diseases. For example, HLA-E restricted T cells have been identified in responses to bacteria and viruses, including Mycobacterium tuberculosis (Mtb) and cytomegalovirus (CMV) (88,89). In mice, H2-M3 restricted T cells have a characteristic pre-activated phenotype, and mediate early T cell responses against Listeria monocytogenes (90).…”

Section: Do the Biases Of Tcrs For Recognition Of Mhc Apply To Nonclamentioning

confidence: 99%

Evolutionarily Conserved Amino Acids That Control TCR-MHC Interaction

Marrack

Scott‐Browne

Dai

et al. 2008

Annu. Rev. Immunol.

252

341

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Alpha/beta T cell receptors (TCRs) react with major histocompatibility complex proteins (MHC) plus peptides, a poorly understood phenomenon, probably because thymocytes bearing TCRs that manifest MHC-reactivity too well are lost by negative selection. Only TCRs with attenuated ability to react with MHC appear on mature T cells. Also, the interaction sites between TCRs and MHC may be inherently flexible and hence difficult to spot. Contacts between TCRs and MHC in the solved structures of their complexes were reevaluated with these points in mind. The results show that frequently used amino acids in TCR CDR1 and CDR2 regions are often used to bind MHC, in areas around small amino acids on the surfaces of MHC α helices that form a cup, allowing somewhat flexible binding of the TCRs. The TCR amino acids involved are specific to families of V regions and partially different rules govern recognition of MHC1 versus MHCII. TermsT cell receptor; MHC; evolution; conserved interactions; tolerance; selection; major histocompatibility complex A HISTORICAL INTRODUCTIONIt is almost 50 years since the discovery that the thymus had something to do with immune responses. Shortly thereafter, cells derived from the thymus were found to improve the ability of B cells to make antibodies, This was followed by the discovery of the carrier effect, i.e. the observation that the antibody response to haptens requires simultaneous recognition of both the hapten and epitopes on the attached protein carrier. These findings dovetailed unexpectedly well to give rise to the idea that T cells created in the thymus react with one portion of the antigen and then help B cells make antibody against a different determinant on the same molecule (1-4). This satisfying explanation for cell cooperation in NIH Public Access Author ManuscriptAnnu Rev Immunol. Author manuscript; available in PMC 2011 September 1.Published in final edited form as: Annu Rev Immunol. 2008 ; 26: 171-203. doi:10.1146/annurev.immunol.26.021607.090421. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscriptimmune responses left unresolved one key problem for immunologists, the problem of the major histocompatibility complex.The fact that the major histocompatibility complex (MHC) represents a special case for immune responses had been recognized many years before, by people studying the rejection of grafts and tumors (5, 6). They found that differences at the MHC were recognized by the immune system extraordinarily rapidly. This phenomenon led Niels Jerne to propose that lymphocyte receptors, by which, at the time, he meant immunoglobulin proteins, had evolved evolutionary to react with alleles of the MHC (7). In a ground breaking theoretical paper, he suggested that lymphocytes developing in the thymus somatically mutate their evolutionarily generated receptors such that the receptors no longer react with the MHC of their host, but retain the ability to react well with MHC of others.Meanwhile, others were beginning to realize that T and B cells do not re...

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“…This enhances expression of HLA-E, which is an inhibitory ligand of CD94/NKG2a. HLA-E-restricted CD8 T-cell responses have been demonstrated in healthy donors (92). Mutimer et al (101) created CD4 and CD8 T-cell clones from the vitreous humor of one patient.…”

Section: Ird Manifested As CMV Retinitis or Viral Encephalomyelitis: mentioning

confidence: 99%

Immune Restoration Diseases Reflect Diverse Immunopathological Mechanisms

et al. 2009

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SUMMARY Up to one in four patients infected with human immunodeficiency virus type 1 and given antiretroviral therapy (ART) experiences inflammatory or cellular proliferative disease associated with a preexisting opportunistic infection, which may be subclinical. These immune restoration diseases (IRD) appear to result from the restoration of immunocompetence. IRD associated with intracellular pathogens are characterized by cellular immune responses and/or granulomatous inflammation. Mycobacterial and cryptococcal IRD are attributed to a pathological overproduction of Th1 cytokines. Clinicopathological characteristics of IRD associated with viral infections suggest different pathogenic mechanisms. For example, IRD associated with varicella-zoster virus or JC polyomavirus infection correlate with a CD8 T-cell response in the central nervous system. Exacerbations or de novo presentations of hepatitis associated with hepatitis C virus (HCV) infection following ART may also reflect restoration of pathogen-specific immune responses as titers of HCV-reactive antibodies rise in parallel with liver enzymes and plasma markers of T-cell activation. Correlations between immunological parameters assessed in longitudinal sample sets and clinical presentations are required to illuminate the diverse immunological scenarios described collectively as IRD. Here we present salient clinical features and review progress toward understanding their pathogeneses.

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Identification of effector-memory CMV-specific T lymphocytes that kill CMV-infected target cells in an HLA-E-restricted fashion

Cited by 75 publications

References 44 publications

Extensive HLA class I allele promiscuity among viral CTL epitopes

Extensive HLA class I allele promiscuity among viral CTL epitopes

Evolutionarily Conserved Amino Acids That Control TCR-MHC Interaction

Immune Restoration Diseases Reflect Diverse Immunopathological Mechanisms

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