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Article ; Online: Role of CD4+ T Cells in the Control of Viral Infections: Recent Advances and Open Questions.

Kervevan, Jérôme / Chakrabarti, Lisa A

International journal of molecular sciences

2021 Volume 22, Issue 2

Abstract: CD4+ T cells orchestrate adaptive immune responses through their capacity to recruit and provide help to multiple immune effectors, in addition to exerting direct effector functions. CD4+ T cells are increasingly recognized as playing an essential role ... ...

Abstract	CD4+ T cells orchestrate adaptive immune responses through their capacity to recruit and provide help to multiple immune effectors, in addition to exerting direct effector functions. CD4+ T cells are increasingly recognized as playing an essential role in the control of chronic viral infections. In this review, we present recent advances in understanding the nature of CD4+ T cell help provided to antiviral effectors. Drawing from our studies of natural human immunodeficiency virus (HIV) control, we then focus on the role of high-affinity T cell receptor (TCR) clonotypes in mediating antiviral CD4+ T cell responses. Last, we discuss the role of TCR affinity in determining CD4+ T cell differentiation, reviewing the at times divergent studies associating TCR signal strength to the choice of a T helper 1 (Th1) or a T follicular helper (Tfh) cell fate.
MeSH term(s)	Adaptive Immunity/immunology ; CD8-Positive T-Lymphocytes/immunology ; Cell Differentiation/immunology ; HIV Infections/immunology ; HIV Infections/virology ; Humans ; Immunity, Humoral/immunology ; Receptors, Antigen, T-Cell/immunology ; T Follicular Helper Cells/cytology ; T Follicular Helper Cells/immunology ; T-Lymphocytes, Regulatory/immunology
Chemical Substances	Receptors, Antigen, T-Cell
Language	English
Publishing date	2021-01-07
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms22020523
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Article ; Online: Recapitulating memory B cell responses in a Lymphoid Organ-Chip to evaluate mRNA vaccine boosting strategies

Jeger-Madiot, Raphaël / Planas, Delphine / Staropoli, Isabelle / Kervevan, Jérôme / Mary, Héloïse / Collina, Camilla / Fonseca, Barbara F. / Debarnot, Hippolyte / Robinot, Rémy / Gellenoncourt, Stacy / Schwartz, Olivier / Ewart, Lorna / Bscheider, Michael / Gobaa, Samy / Chakrabarti, Lisa A.

bioRxiv

Abstract: Predicting the immunogenicity of candidate vaccines in humans remains a challenge. To address this issue, we developed a Lymphoid Organ-Chip (LO chip) model based on a microfluidic chip seeded with human PBMC at high density within a 3D collagen matrix. ... ...

Abstract	Predicting the immunogenicity of candidate vaccines in humans remains a challenge. To address this issue, we developed a Lymphoid Organ-Chip (LO chip) model based on a microfluidic chip seeded with human PBMC at high density within a 3D collagen matrix. Perfusion of the SARS-CoV-2 Spike protein mimicked a vaccine boost by inducing a massive amplification of Spike-specific memory B cells, plasmablast differentiation, and Spike-specific antibody secretion. Features of lymphoid tissue, including the formation of activated CD4+ T cell/B cell clusters and the emigration of matured plasmablasts, were recapitulated in the LO chip. Importantly, myeloid cells were competent at capturing and expressing mRNA vectored by lipid nanoparticles, enabling the assessment of responses to mRNA vaccines. Comparison of on-chip responses to Wuhan monovalent and Wuhan/Omicron bivalent mRNA vaccine boosts showed equivalent induction of Omicron neutralizing antibodies, pointing at immune imprinting as reported in vivo. The LO chip thus represents a versatile platform suited to the preclinical evaluation of vaccine boosting strategies.
Keywords	covid19
Language	English
Publishing date	2024-02-02
Publisher	Cold Spring Harbor Laboratory
Document type	Article ; Online
DOI	10.1101/2024.02.02.578553
Database	COVID19

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Article ; Online: Divergent adaptive immune responses define two types of long COVID.

Kervevan, Jérôme / Staropoli, Isabelle / Slama, Dorsaf / Jeger-Madiot, Raphaël / Donnadieu, Françoise / Planas, Delphine / Pietri, Marie-Pierre / Loghmari-Bouchneb, Wiem / Alaba Tanah, Motolete / Robinot, Rémy / Boufassa, Faroudy / White, Michael / Salmon-Ceron, Dominique / Chakrabarti, Lisa A

Frontiers in immunology

2023 Volume 14, Page(s) 1221961

Abstract: Background: The role of adaptive immune responses in long COVID remains poorly understood, with contrasting hypotheses suggesting either an insufficient antiviral response or an excessive immune response associated with inflammatory damage. To address ... ...

Abstract	Background: The role of adaptive immune responses in long COVID remains poorly understood, with contrasting hypotheses suggesting either an insufficient antiviral response or an excessive immune response associated with inflammatory damage. To address this issue, we set to characterize humoral and CD4+ T cell responses in long COVID patients prior to SARS-CoV-2 vaccination. Methods: Long COVID patients who were seropositive (LC+, n=28) or seronegative (LC-, n=23) by spike ELISA assay were recruited based on (i) an initial SARS-CoV-2 infection documented by PCR or the conjunction of three major signs of COVID-19 and (ii) the persistence or resurgence of at least 3 symptoms for over 3 months. They were compared to COVID patients with resolved symptoms (RE, n=29) and uninfected control individuals (HD, n=29). Results: The spectrum of persistent symptoms proved similar in both long COVID groups, with a trend for a higher number of symptoms in the seronegative group (median=6 Conclusions: These findings provide evidence for two major types of antiviral immune responses in long COVID. Seropositive patients showed coordinated cellular and humoral responses at least as high as those of recovered patients. In contrast, ELISA-seronegative long COVID patients showed overall low antiviral responses, with detectable specific CD4+ T cells and/or antibodies in close to half of patients (52.2%). These divergent findings in patients sharing a comparable spectrum of persistent symptoms raise the possibility of multiple etiologies in long COVID.
MeSH term(s)	Humans ; Post-Acute COVID-19 Syndrome ; COVID-19 ; COVID-19 Vaccines ; SARS-CoV-2 ; Antibodies, Viral ; Antiviral Agents ; Immunoglobulin G
Chemical Substances	COVID-19 Vaccines ; Antibodies, Viral ; Antiviral Agents ; Immunoglobulin G
Language	English
Publishing date	2023-07-20
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2023.1221961
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Article ; Online: The Spike-Stabilizing D614G Mutation Interacts with S1/S2 Cleavage Site Mutations To Promote the Infectious Potential of SARS-CoV-2 Variants.

Gellenoncourt, Stacy / Saunders, Nell / Robinot, Rémy / Auguste, Lucas / Rajah, Maaran Michael / Kervevan, Jérôme / Jeger-Madiot, Raphaël / Staropoli, Isabelle / Planchais, Cyril / Mouquet, Hugo / Buchrieser, Julian / Schwartz, Olivier / Chakrabarti, Lisa A

Journal of virology

2022 Volume 96, Issue 19, Page(s) e0130122

Abstract: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) remained genetically stable during the first 3 months of the pandemic, before acquiring a D614G spike mutation that rapidly spread worldwide and then generating successive waves of viral ... ...

Abstract	Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) remained genetically stable during the first 3 months of the pandemic, before acquiring a D614G spike mutation that rapidly spread worldwide and then generating successive waves of viral variants with increasingly high transmissibility. We set out to evaluate possible epistatic interactions between the early-occurring D614G mutation and the more recently emerged cleavage site mutations present in spike of the Alpha, Delta, and Omicron variants of concern. The P681H/R mutations at the S1/S2 cleavage site increased spike processing and fusogenicity but limited its incorporation into pseudoviruses. In addition, the higher cleavage rate led to higher shedding of the spike S1 subunit, resulting in a lower infectivity of the P681H/R-carrying pseudoviruses compared to those expressing the Wuhan wild-type spike. The D614G mutation increased spike expression at the cell surface and limited S1 shedding from pseudovirions. As a consequence, the D614G mutation preferentially increased the infectivity of P681H/R-carrying pseudoviruses. This enhancement was more marked in cells where the endosomal route predominated, suggesting that more stable spikes could better withstand the endosomal environment. Taken together, these findings suggest that the D614G mutation stabilized S1/S2 association and enabled the selection of mutations that increased S1/S2 cleavage, leading to the emergence of SARS-CoV-2 variants expressing highly fusogenic spikes.
MeSH term(s)	COVID-19/virology ; Humans ; Mutation ; SARS-CoV-2/genetics ; SARS-CoV-2/pathogenicity ; Spike Glycoprotein, Coronavirus/genetics
Chemical Substances	Spike Glycoprotein, Coronavirus ; spike protein, SARS-CoV-2
Language	English
Publishing date	2022-09-19
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80174-4
ISSN	1098-5514 ; 0022-538X
ISSN (online)	1098-5514
ISSN	0022-538X
DOI	10.1128/jvi.01301-22
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Article ; Online: The spike-stabilizing D614G mutation interacts with S1/S2 cleavage site mutations to promote the infectious potential of SARS-CoV-2 variants

Gellenoncourt, Stacy / Saunders, Nell / Robinot, Remy / Auguste, Lucas / Rajah, Maaran Michael / Kervevan, Jerome / Jeger-Madiot, Raphael / Staropoli, Isabelle / Planchais, Cyril / Mouquet, Hugo / Buchrieser, Julian / Schwartz, Olivier / Chakrabarti, Lisa A.

bioRxiv

Abstract: SARS-CoV-2 remained genetically stable during the first three months of the pandemic, before acquiring a D614G spike mutation that rapidly spread worldwide, and then generating successive waves of viral variants with increasingly high transmissibility. ... ...

Abstract	SARS-CoV-2 remained genetically stable during the first three months of the pandemic, before acquiring a D614G spike mutation that rapidly spread worldwide, and then generating successive waves of viral variants with increasingly high transmissibility. We set out to evaluate possible epistatic interactions between the early occurring D614G mutation and the more recently emerged cleavage site mutations present in spike of the Alpha, Delta, and Omicron variants of concern. The P681H/R mutations at the S1/S2 cleavage site increased spike processing and fusogenicity but limited its incorporation into pseudoviruses. In addition, the higher cleavage rate led to higher shedding of the spike S1 subunit, resulting in a lower infectivity of the P681H/R-carrying pseudoviruses compared to those expressing the Wuhan wild-type spike. The D614G mutation increased spike expression at the cell surface and limited S1 shedding from pseudovirions. As a consequence, the D614G mutation preferentially increased the infectivity of P681H/R-carrying pseudoviruses. This enhancement was more marked in cells where the endosomal route predominated, suggesting that more stable spikes could better withstand the endosomal environment. Taken together, these findings suggest that the D614G mutation stabilized S1/S2 association and enabled the selection of mutations that increased S1/S2 cleavage, leading to the emergence of SARS-CoV-2 variants expressing highly fusogenic spikes.
Keywords	covid19
Language	English
Publishing date	2022-05-20
Publisher	Cold Spring Harbor Laboratory
Document type	Article ; Online
DOI	10.1101/2022.05.20.492832
Database	COVID19

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Article ; Online: Low CCR5 expression protects HIV-specific CD4+ T cells of elite controllers from viral entry.

Claireaux, Mathieu / Robinot, Rémy / Kervevan, Jérôme / Patgaonkar, Mandar / Staropoli, Isabelle / Brelot, Anne / Nouël, Alexandre / Gellenoncourt, Stacy / Tang, Xian / Héry, Mélanie / Volant, Stevenn / Perthame, Emeline / Avettand-Fenoël, Véronique / Buchrieser, Julian / Cokelaer, Thomas / Bouchier, Christiane / Ma, Laurence / Boufassa, Faroudy / Hendou, Samia /

Libri, Valentina / Hasan, Milena / Zucman, David / de Truchis, Pierre / Schwartz, Olivier / Lambotte, Olivier / Chakrabarti, Lisa A

Nature communications

2022 Volume 13, Issue 1, Page(s) 521

Abstract: HIV elite controllers maintain a population of CD4 + T cells endowed with high avidity for Gag antigens and potent effector functions. How these HIV-specific cells avoid infection and depletion upon encounter with the virus remains incompletely ... ...

Abstract	HIV elite controllers maintain a population of CD4 + T cells endowed with high avidity for Gag antigens and potent effector functions. How these HIV-specific cells avoid infection and depletion upon encounter with the virus remains incompletely understood. Ex vivo characterization of single Gag-specific CD4 + T cells reveals an advanced Th1 differentiation pattern in controllers, except for the CCR5 marker, which is downregulated compared to specific cells of treated patients. Accordingly, controller specific CD4 + T cells show decreased susceptibility to CCR5-dependent HIV entry. Two controllers carried biallelic mutations impairing CCR5 surface expression, indicating that in rare cases CCR5 downregulation can have a direct genetic cause. Increased expression of β-chemokine ligands upon high-avidity antigen/TCR interactions contributes to autocrine CCR5 downregulation in controllers without CCR5 mutations. These findings suggest that genetic and functional regulation of the primary HIV coreceptor CCR5 play a key role in promoting natural HIV control.
MeSH term(s)	CD4-Positive T-Lymphocytes/immunology ; Chemokines ; Down-Regulation ; Elite Controllers ; Gene Expression Regulation ; Gene Products, gag/metabolism ; HIV Infections/immunology ; HIV Infections/virology ; HIV-1/immunology ; Histocompatibility Antigens Class II ; Humans ; Mutation ; Receptors, CCR5/genetics ; Receptors, CCR5/metabolism ; Receptors, CXCR3 ; Virus Internalization
Chemical Substances	CCR5 protein, human ; CXCR3 protein, human ; Chemokines ; Gene Products, gag ; Histocompatibility Antigens Class II ; Receptors, CCR5 ; Receptors, CXCR3
Language	English
Publishing date	2022-01-26
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-022-28130-0
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: DC Subsets Regulate Humoral Immune Responses by Supporting the Differentiation of Distinct Tfh Cells.

Bouteau, Aurélie / Kervevan, Jérôme / Su, Qingtai / Zurawski, Sandra M / Contreras, Vanessa / Dereuddre-Bosquet, Nathalie / Le Grand, Roger / Zurawski, Gerard / Cardinaud, Sylvain / Levy, Yves / Igyártó, Botond Z

Frontiers in immunology

2019 Volume 10, Page(s) 1134

Abstract: To determine the contribution of skin DC subsets in the regulation of humoral immunity, we used a well-characterized antigen targeting system to limit antigen availability and presentation to certain skin-derived DC subsets. Here we show that delivery of ...

Abstract	To determine the contribution of skin DC subsets in the regulation of humoral immunity, we used a well-characterized antigen targeting system to limit antigen availability and presentation to certain skin-derived DC subsets. Here we show that delivery of foreign antigen to steady state Langerhans cells (LCs) and cDC1s through the same receptor (Langerin) led to, respectively, robust vs. minimal-to-null humoral immune response. LCs, unlike cDC1s, supported the formation of germinal center T follicular helper cells (GC-Tfh) antigen dose-dependently and then, likely licensed by these T cells, some of the LCs migrated to the B cell area to initiate B cell responses. Furthermore, we found that the cDC1s, probably through their superior T cell activation capacity, prevented the LCs from inducing GC-Tfh cells and humoral immune responses. We further show that targeted delivery of cytokines to DCs can be used to modulate DC-induced humoral immune responses, which has important therapeutic potential. Finally, we show that human LCs, unlike monocyte-derived DCs, can support GC Tfh generation in an
MeSH term(s)	Adoptive Transfer ; Animals ; B-Lymphocytes/immunology ; Cell Differentiation ; Dendritic Cells/immunology ; Female ; HIV Core Protein p24/immunology ; Humans ; Immunity, Humoral ; Lymph Nodes/immunology ; Macaca fascicularis ; Male ; Mice, Transgenic ; Skin/cytology ; Skin/immunology ; T-Lymphocytes, Helper-Inducer/immunology
Chemical Substances	HIV Core Protein p24
Language	English
Publishing date	2019-05-27
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2019.01134
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Article ; Online: Targeting human langerin promotes HIV-1 specific humoral immune responses.

PLoS pathogens

2021 Volume 17, Issue 7, Page(s) e1009749

Abstract: The main avenue for the development of an HIV-1 vaccine remains the induction of protective antibodies. A rationale approach is to target antigen to specific receptors on dendritic cells (DC) via fused monoclonal antibodies (mAb). In mouse and non-human ... ...

Abstract	The main avenue for the development of an HIV-1 vaccine remains the induction of protective antibodies. A rationale approach is to target antigen to specific receptors on dendritic cells (DC) via fused monoclonal antibodies (mAb). In mouse and non-human primate models, targeting of skin Langerhans cells (LC) with anti-Langerin mAbs fused with HIV-1 Gag antigen drives antigen-specific humoral responses. The development of these immunization strategies in humans requires a better understanding of early immune events driven by human LC. We therefore produced anti-Langerin mAbs fused with the HIV-1 gp140z Envelope (αLC.Env). First, we show that primary skin human LC and in vitro differentiated LC induce differentiation and expansion of naïve CD4+ T cells into T follicular helper (Tfh) cells. Second, when human LC are pre-treated with αLC.Env, differentiated Tfh cells significantly promote the production of specific IgG by B cells. Strikingly, HIV-Env-specific Ig are secreted by HIV-specific memory B cells. Consistently, we found that receptors and cytokines involved in Tfh differentiation and B cell functions are upregulated by LC during their maturation and after targeting Langerin. Finally, we show that subcutaneous immunization of mice by αLC.Env induces germinal center (GC) reaction in draining lymph nodes with higher numbers of Tfh cells, Env-specific B cells, as well as specific IgG serum levels compared to mice immunized with the non-targeting Env antigen. Altogether, we provide evidence that human LC properly targeted may be licensed to efficiently induce Tfh cell and B cell responses in GC.
MeSH term(s)	AIDS Vaccines/immunology ; Animals ; Antigens, CD/immunology ; HIV-1/immunology ; Humans ; Immunity, Humoral/immunology ; Langerhans Cells/immunology ; Lectins, C-Type/immunology ; Lymphocyte Activation/immunology ; Mannose-Binding Lectins/immunology ; Mice ; env Gene Products, Human Immunodeficiency Virus/immunology
Chemical Substances	AIDS Vaccines ; Antigens, CD ; CD207 protein, human ; Lectins, C-Type ; Mannose-Binding Lectins ; env Gene Products, Human Immunodeficiency Virus ; gp140 envelope protein, Human immunodeficiency virus 1
Language	English
Publishing date	2021-07-29
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2205412-1
ISSN	1553-7374 ; 1553-7366
ISSN (online)	1553-7374
ISSN	1553-7366
DOI	10.1371/journal.ppat.1009749
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Article ; Online: Triggering of TLR-3, -4, NOD2, and DC-SIGN reduces viral replication and increases T-cell activation capacity of HIV-infected human dendritic cells.

Cardinaud, Sylvain / Urrutia, Alejandra / Rouers, Angeline / Coulon, Pierre-Grégoire / Kervevan, Jérome / Richetta, Clémence / Bet, Anne / Maze, Emmanuel A / Larsen, Martin / Iglesias, Maria-Candela / Appay, Victor / Graff-Dubois, Stéphanie / Moris, Arnaud

European journal of immunology

2017 Volume 47, Issue 5, Page(s) 818–829

Abstract: A variety of signals influence the capacity of dendritic cells (DCs) to mount potent antiviral cytotoxic T-cell (CTL) responses. In particular, innate immune sensing by pathogen recognition receptors, such as TLR and C-type lectines, influences DC ... ...

Abstract	A variety of signals influence the capacity of dendritic cells (DCs) to mount potent antiviral cytotoxic T-cell (CTL) responses. In particular, innate immune sensing by pathogen recognition receptors, such as TLR and C-type lectines, influences DC biology and affects their susceptibility to HIV infection. Yet, whether the combined effects of PPRs triggering and HIV infection influence HIV-specific (HS) CTL responses remain enigmatic. Here, we dissect the impact of innate immune sensing by pathogen recognition receptors on DC maturation, HIV infection, and on the quality of HS CTL activation. Remarkably, ligand-driven triggering of TLR-3, -4, NOD2, and DC-SIGN, despite reducing viral replication, markedly increased the capacity of infected DCs to stimulate HS CTLs. This was exemplified by the diversity and the quantity of cytokines produced by HS CTLs primed by these DCs. Infecting DCs with viruses harboring members of the APOBEC family of antiviral factors enhanced the antigen-presenting skills of infected DCs. Our results highlight the tight interplay between innate and adaptive immunity and may help develop innovative immunotherapies against viral infections.
MeSH term(s)	APOBEC Deaminases ; Antigen Presentation ; Cell Adhesion Molecules/genetics ; Cell Adhesion Molecules/immunology ; Cell Adhesion Molecules/metabolism ; Cytidine Deaminase ; Cytosine Deaminase/genetics ; Cytosine Deaminase/metabolism ; Dendritic Cells/immunology ; Dendritic Cells/physiology ; Dendritic Cells/virology ; HIV-1/immunology ; HIV-1/physiology ; Humans ; Lectins, C-Type/genetics ; Lectins, C-Type/immunology ; Lectins, C-Type/metabolism ; Lymphocyte Activation ; Nod2 Signaling Adaptor Protein/genetics ; Nod2 Signaling Adaptor Protein/immunology ; Nod2 Signaling Adaptor Protein/metabolism ; Pathogen-Associated Molecular Pattern Molecules ; Receptors, Cell Surface/genetics ; Receptors, Cell Surface/immunology ; Receptors, Cell Surface/metabolism ; T-Lymphocytes, Cytotoxic/immunology ; Toll-Like Receptor 3/genetics ; Toll-Like Receptor 3/immunology ; Toll-Like Receptor 3/metabolism ; Toll-Like Receptor 4/genetics ; Toll-Like Receptor 4/immunology ; Toll-Like Receptor 4/metabolism ; Virus Replication
Chemical Substances	Cell Adhesion Molecules ; DC-specific ICAM-3 grabbing nonintegrin ; Lectins, C-Type ; NOD2 protein, human ; Nod2 Signaling Adaptor Protein ; Pathogen-Associated Molecular Pattern Molecules ; Receptors, Cell Surface ; TLR3 protein, human ; TLR4 protein, human ; Toll-Like Receptor 3 ; Toll-Like Receptor 4 ; Cytosine Deaminase (EC 3.5.4.1) ; APOBEC Deaminases (EC 3.5.4.5) ; APOBEC3 proteins, human (EC 3.5.4.5) ; Cytidine Deaminase (EC 3.5.4.5)
Language	English
Publishing date	2017-04-13
Publishing country	Germany
Document type	Journal Article
ZDB-ID	120108-6
ISSN	1521-4141 ; 0014-2980
ISSN (online)	1521-4141
ISSN	0014-2980
DOI	10.1002/eji.201646603
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