Impaired intracellular transport of class I MHC antigens as a possible means for adenoviruses to evade immune surveillance

Andersson, Matilda; Pääbo, Svante; Nilsson, Tommy; Peterson, Per A.

doi:10.1016/0092-8674(85)90026-1

Cited by 305 publications

(167 citation statements)

References 34 publications

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“…The HLA-G-specific mAb G233 was a gift from Dr. Y. Loke (University of Cambridge, Cambridge, U.K.). Polyclonal rabbit K455 Ab reacts with MHC class I H chains and ␤ 2 m in both assembled and nonassembled forms (15). The mouse mAb HLA-B Ab-1 (NeoMarkers, Fremont, CA) recognizes only HLA-B alleles and mAb W6/32 recognizes only the complex of H chain and ␤ 2 m. The anti-tapasin Ab (R.gp48N) was a gift from Dr. P. Cresswell (Yale University, New Haven, CT).…”

Section: Stable Cell Lines and Absmentioning

confidence: 99%

A Single Polymorphic Residue Within the Peptide-Binding Cleft of MHC Class I Molecules Determines Spectrum of Tapasin Dependence

Park

Lee

Kim

et al. 2003

The Journal of Immunology

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Different HLA class I alleles display a distinctive dependence on tapasin for surface expression and Ag presentation. In this study, we show that the tapasin dependence of HLA class I alleles correlates to the nature of the amino acid residues present at the naturally polymorphic position 114. The tapasin dependence of HLA class I alleles bearing different residues at position 114 decreases in the order of acidity, with high tapasin dependence for acidic amino acids (aspartic acid and glutamic acid), moderate dependence for neutral amino acids (asparagine and glutamine), and low dependence for basic amino acids (histidine and arginine). A glutamic acid to histidine substitution at position 114 allows the otherwise tapasin-dependent HLA-B4402 alleles to load high-affinity peptides independently of tapasin and to have surface expression levels comparable to the levels seen in the presence of tapasin. The opposite substitution, histidine to glutamic acid at position 114, is sufficient to change the HLA-B2705 allele from the tapasin-independent to the tapasin-dependent phenotype. Furthermore, analysis of point mutants at position 114 reveals that tapasin plays a principal role in transforming the peptide-binding groove into a high-affinity, peptide-receptive conformation. The natural polymorphisms in HLA class I H chains that selectively affect tapasin-dependent peptide loading provide insights into the functional interaction of tapasin with MHC class I molecules.

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Section: Stable Cell Lines and Absmentioning

confidence: 99%

A Single Polymorphic Residue Within the Peptide-Binding Cleft of MHC Class I Molecules Determines Spectrum of Tapasin Dependence

Park

Lee

Kim

et al. 2003

The Journal of Immunology

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“…APLP2 was detected at equivalent levels on HeLa and HeLa-etK d (Fig. 3) is known to bind to class I molecules and retain them in the ER through an ER retrieval sequence in its cytoplasmic tail (21,44,45). E3/19K also binds independently to TAP and thereby prevents tapasin from bridging TAP to class I (46).…”

Section: Aplp2mentioning

confidence: 95%

The Amyloid Precursor-like Protein 2 and the Adenoviral E3/19K Protein Both Bind to a Conformational Site on H-2Kd and Regulate H-2Kd Expression

Morris

Petersen

Vargas

et al. 2003

Journal of Biological Chemistry

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“…This molecule inhibits the formation of TAP-MHCI complex by interfering with the transport of MHCI to the plasma membrane. 49,50 Consequently, adenovirus is able to replicate in a prolific manner in tumor cells since infected cells are not killed by anti-viral Tcells.…”

Section: Discussionmentioning

confidence: 99%

Intravenously usable fully serotype 3 oncolytic adenovirus coding for CD40L as an enabler of dendritic cell therapy

et al. 2017

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Vaccination with dendritic cells (DCs), the most potent professional antigen-presenting cells in the body, is a promising approach in cancer immunotherapy. However, tumors induce immunosuppression in their microenvironment that suppresses and impairs the function of DCs. Therefore, human clinical trials with DC therapy have often been disappointing. To improve the therapeutic efficacy and to overcome the major obstacles of DC therapy, we generated a novel adenovirus, Ad3-hTERT-CMV-hCD40L, which is fully serotype 3 and expresses hCD40L for induction of antitumor immune response. The specific aim is to enhance DCs function. Data from a human cancer patient indicated that this capsid allows effective transduction of distant tumors through the intravenous route. Moreover, patient data suggested that virally produced hCD40L can activate DCs in situ. The virus was efficient in vitro and had potent antitumor activity in vivo. In a syngeneic model, tumors treated with Ad5/3-CMV-mCD40L virus plus DCs elicited greater antitumor effect as compared with either treatment alone. Moreover, virally coded CD40L induced activation of DCs, which in turn, lead to the induction of a Th1 immune response and increased tumorspecific T cells. In conclusion, Ad3-hTERT-CMV-hCD40L is promising for translation into human trials. In particular, this virus could enable successful dendritic cell therapy in cancer patients.

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Impaired intracellular transport of class I MHC antigens as a possible means for adenoviruses to evade immune surveillance

Cited by 305 publications

References 34 publications

A Single Polymorphic Residue Within the Peptide-Binding Cleft of MHC Class I Molecules Determines Spectrum of Tapasin Dependence

A Single Polymorphic Residue Within the Peptide-Binding Cleft of MHC Class I Molecules Determines Spectrum of Tapasin Dependence

The Amyloid Precursor-like Protein 2 and the Adenoviral E3/19K Protein Both Bind to a Conformational Site on H-2Kd and Regulate H-2Kd Expression

Intravenously usable fully serotype 3 oncolytic adenovirus coding for CD40L as an enabler of dendritic cell therapy

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