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Article ; Online: Mitochondrial ROS and base excision repair steps leading to DNA nick formation drive ultraviolet induced-NETosis.

Azzouz, Dhia / Palaniyar, Nades

2023 Volume 14, Page(s) 1198716

Abstract: Reactive oxygen species (ROS) is essential for neutrophil extracellular trap formation (NETosis), and generated either by NADPH oxidases (e.g., during infections) or mitochondria (e.g., sterile injury) in neutrophils. We recently showed that ultraviolet ( ...

Abstract	Reactive oxygen species (ROS) is essential for neutrophil extracellular trap formation (NETosis), and generated either by NADPH oxidases (e.g., during infections) or mitochondria (e.g., sterile injury) in neutrophils. We recently showed that ultraviolet (UV) radiation, a sterile injury-inducing agent, dose-dependently induced mitochondrial ROS generation, and increasing levels of ROS shifted the neutrophil death from apoptosis to NETosis. Nevertheless, how ROS executes UV-induced NETosis is unknown. In this study, we first confirmed that UV doses used in our experiments generated mitochondrial ROS, and the inhibition of mitochondrial ROS suppressed NETosis (Mitosox, SYTOX, immunocytochemistry, imaging). Next, we showed that UV irradiation extensively oxidized DNA, by confocal imaging of 8-oxyguanine (8-oxoG) in NETs. Immunofluorescence microscopy further showed that a DNA repair protein, proliferating cell nuclear antigen, was widely distributed throughout the DNA, indicating that the DNA repair machinery was active throughout the genome during UV-induced NETosis. Inhibition of specific steps of base excision repair (BER) pathway showed that steps leading up to DNA nick formation, but not the later steps, suppressed UV-induced NETosis. In summary, this study shows that (i) high levels of mitochondrial ROS produced following UV irradiation induces extensive oxidative DNA damage, and (ii) early steps of the BER pathway leading to DNA nicking results in chromatin decondensation and NETosis. Collectively, these findings reveal how ROS induces NOX-independent NETosis, and also a novel biological mechanism for UV irradiation- and -mitochondrial ROS-mediated NETosis.
MeSH term(s)	Reactive Oxygen Species/metabolism ; DNA Breaks, Single-Stranded ; Mitochondria/genetics ; Mitochondria/metabolism ; DNA/metabolism ; DNA Repair
Chemical Substances	Reactive Oxygen Species ; DNA (9007-49-2)
Language	English
Publishing date	2023-06-07
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.2023.1198716
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Article ; Online: ROS and DNA repair in spontaneous versus agonist-induced NETosis: Context matters.

Azzouz, Dhia / Palaniyar, Nades

Frontiers in immunology

2022 Volume 13, Page(s) 1033815

Abstract: Reactive oxygen species (ROS) is essential for neutrophil extracellular trap formation (NETosis). Nevertheless, how ROS induces NETosis at baseline and during neutrophil activation is unknown. Although neutrophils carry DNA transcription, replication and ...

Abstract	Reactive oxygen species (ROS) is essential for neutrophil extracellular trap formation (NETosis). Nevertheless, how ROS induces NETosis at baseline and during neutrophil activation is unknown. Although neutrophils carry DNA transcription, replication and repair machineries, their relevance in the short-lived mature neutrophils that carry pre-synthesized proteins has remained a mystery for decades. Our recent studies show that (i) NETosis-inducing agonists promote NETosis-specific kinase activation, genome-wide transcription that helps to decondense chromatin, and (ii) excess ROS produced by NADPH oxidase activating agonists generate genome-wide 8-oxy-guanine (8-OG), and the initial steps of DNA repair are needed to decondense chromatin in these cells. These steps require DNA repair proteins necessary for the assembly and nicking at the damaged DNA sites (poly ADP ribose polymerase PARP, apurinic endonuclease APE1 and DNA ligase), but not the enzymes that mediate the repair DNA synthesis (Proliferating cell nuclear antigen (PCNA) and DNA Polymerases). In this study, we show that (i) similar to agonist-induced NETosis, inhibition of early steps of oxidative DNA damage repair proteins suppresses spontaneous NETosis, but (ii) the inhibition of late stage repair proteins DNA polymerases and PCNA drastically promotes baseline NETosis. Hence, in the absence of excessive ROS generation and neutrophil activation, DNA repair mediated by PCNA and DNA polymerases is essential to prevent chromatin decondensation and spontaneous NETosis. These findings indicate that ROS, oxidative DNA damage, transcription and DNA repair differentially regulate spontaneous and agonist-induced NETosis. Therefore, context matters.
MeSH term(s)	Proliferating Cell Nuclear Antigen ; Reactive Oxygen Species ; DNA Repair ; DNA-(Apurinic or Apyrimidinic Site) Lyase ; Chromatin
Chemical Substances	Proliferating Cell Nuclear Antigen ; Reactive Oxygen Species ; DNA-(Apurinic or Apyrimidinic Site) Lyase (EC 4.2.99.18) ; Chromatin
Language	English
Publishing date	2022-11-08
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.2022.1033815
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Article: ROS induces NETosis by oxidizing DNA and initiating DNA repair.

Azzouz, Dhia / Khan, Meraj A / Palaniyar, Nades

Cell death discovery

2021 Volume 7, Issue 1, Page(s) 113

Abstract: Reactive oxygen species (ROS) are essential for neutrophil extracellular trap (NET) formation or NETosis. Nevertheless, how ROS induces NETosis is unknown. Neutrophil activation induces excess ROS production and a meaningless genome-wide transcription to ...

Abstract	Reactive oxygen species (ROS) are essential for neutrophil extracellular trap (NET) formation or NETosis. Nevertheless, how ROS induces NETosis is unknown. Neutrophil activation induces excess ROS production and a meaningless genome-wide transcription to facilitate chromatin decondensation. Here we show that the induction of NADPH oxidase-dependent NETosis leads to extensive DNA damage, and the subsequent translocation of proliferating cell nuclear antigen (PCNA), a key DNA repair protein, stored in the cytoplasm into the nucleus. During the activation of NETosis (e.g., by phorbol myristate acetate, Escherichia coli LPS, Staphylococcus aureus (RN4220), or Pseudomonas aeruginosa), preventing the DNA-repair-complex assembly leading to nick formation that decondenses chromatin causes the suppression of NETosis (e.g., by inhibitors to, or knockdown of, Apurinic endonuclease APE1, poly ADP ribose polymerase PARP, and DNA ligase). The remaining repair steps involving polymerase activity and PCNA interactions with DNA polymerases β/δ do not suppress agonist-induced NETosis. Therefore, excess ROS produced during neutrophil activation induces NETosis by inducing extensive DNA damage (e.g., oxidising guanine to 8-oxoguanine), and the subsequent DNA repair pathway, leading to chromatin decondensation.
Language	English
Publishing date	2021-05-18
Publishing country	United States
Document type	Journal Article
ISSN	2058-7716
ISSN	2058-7716
DOI	10.1038/s41420-021-00491-3
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Article ; Online: ApoNETosis: discovery of a novel form of neutrophil death with concomitant apoptosis and NETosis.

Azzouz, Dhia / Palaniyar, Nades

Cell death & disease

2018 Volume 9, Issue 8, Page(s) 839

MeSH term(s)	Apoptosis/radiation effects ; Caspase 3/metabolism ; Cytochromes c/metabolism ; Extracellular Traps/metabolism ; Humans ; Mitochondria/metabolism ; Neutrophils/cytology ; Neutrophils/metabolism ; Reactive Oxygen Species/metabolism ; Ultraviolet Rays ; p38 Mitogen-Activated Protein Kinases/metabolism
Chemical Substances	Reactive Oxygen Species ; Cytochromes c (9007-43-6) ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; Caspase 3 (EC 3.4.22.-)
Language	English
Publishing date	2018-08-06
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/s41419-018-0846-9
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Article: Two-in-one: UV radiation simultaneously induces apoptosis and NETosis.

Azzouz, Dhia / Khan, Meraj A / Sweezey, Neil / Palaniyar, Nades

Cell death discovery

2018 Volume 4, Page(s) 51

Abstract: NETosis is a unique form of neutrophil death that differs from apoptosis and necrosis. However, whether NETosis and apoptosis can occur simultaneously in the same neutrophil is unknown. In this paper, we show that increasing doses of ultraviolet (UV) ... ...

Abstract	NETosis is a unique form of neutrophil death that differs from apoptosis and necrosis. However, whether NETosis and apoptosis can occur simultaneously in the same neutrophil is unknown. In this paper, we show that increasing doses of ultraviolet (UV) irradiation increases NETosis, which is confirmed by myeloperoxidase colocalisation to neutrophil extracellular DNA. Increasing UV irradiation increases caspase 3 activation, mitochondrial reactive oxygen species (ROS) generation and p38, but not ERK, phosphorylation. Inhibition of mitochondrial ROS production and p38 activation, but not NADPH oxidase (NOX) activity, suppresses UV-induced NETosis, indicating that UV induces NOX-independent NETosis. Like classical NOX-dependent and -independent NETosis, UV-induced NETosis requires transcriptional firing for chromatin decondensation. Cell death-specific inhibitor studies indicate that UV-mediated NETosis is not apoptosis, necrosis or necroptosis. Collectively, these studies indicate that increasing doses of UV irradiation induce both apoptosis and NETosis simultaneously, but the ultimate outcome is the induction of a novel form of NOX-independent NETosis, or "ApoNETosis".
Language	English
Publishing date	2018-04-27
Publishing country	United States
Document type	Journal Article
ISSN	2058-7716
ISSN	2058-7716
DOI	10.1038/s41420-018-0048-3
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Article: Ultraviolet irradiation increases green fluorescence of dihydrorhodamine (DHR) 123: false-positive results for reactive oxygen species generation.

Djiadeu, Pascal / Azzouz, Dhia / Khan, Meraj A / Kotra, Lakshmi P / Sweezey, Neil / Palaniyar, Nades

Pharmacology research & perspectives

2017 Volume 5, Issue 2, Page(s) e00303

Abstract: Dihydrorhodamine (DHR) 123 is a fluorophore commonly used for measuring reactive oxygen species (ROS), often after exposing cells to ultraviolet (UV) irradiation or oxidative burst inducers such as Phorbol 12-myristate 13-acetate (PMA). However, the ... ...

Abstract	Dihydrorhodamine (DHR) 123 is a fluorophore commonly used for measuring reactive oxygen species (ROS), often after exposing cells to ultraviolet (UV) irradiation or oxidative burst inducers such as Phorbol 12-myristate 13-acetate (PMA). However, the negative effects of UV irradiation on oxidation of DHR123 itself to green fluorescence rhodamine (R) 123 under different experimental conditions (e.g., different buffers, media, cells, ROS detection techniques) have not been fully appreciated. We determined the effect of UV on DHR123 fluorescence, using a cell-free system, and A549 epithelial cells, NIH/3T3 fibroblast cells, Jurkat T cells, primary human T cells, HL-60 neutrophils and primary human neutrophils. We found that UV irradiation rapidly increases green fluorescence of DHR123 in cell-free solutions. The intensity of green fluorescence increases with increasing amounts of DHR123 and UV exposure. The fluorescence increase was greater in Roswell Park Memorial Institute medium (RPMI) than DMEM media. The presence of DMSO (0-1.25%, v/v) in RPMI further increases the fluorescence signal. Phosphate buffered solution (PBS) and Hanks' Balanced Salt Solution (HBSS) generate considerable background signal with DHR123, and increasing DMSO concentration greatly increases the fluorescence signal in these buffers. However, after UV irradiation the amount of DHR123 that remains unoxidized generates sufficient fluorescence signal to measure the ROS produced by H
Language	English
Publishing date	2017-03-10
Publishing country	United States
Document type	Journal Article
ZDB-ID	2740389-0
ISSN	2052-1707
ISSN	2052-1707
DOI	10.1002/prp2.303
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Article ; Online: Surfactant protein D regulates caspase-8-mediated cascade of the intrinsic pathway of apoptosis while promoting bleb formation.

Djiadeu, Pascal / Farmakovski, Nicole / Azzouz, Dhia / Kotra, Lakshmi P / Sweezey, Neil / Palaniyar, Nades

Molecular immunology

2017 Volume 92, Page(s) 190–198

Abstract: Surfactant-associated protein D (SP-D) is a soluble innate immune collectin present on many mucosal surfaces. We recently showed that SP-D suppresses the extrinsic pathway of apoptosis by downregulating caspase-8 activation. However, the effects of SP-D ... ...

Abstract	Surfactant-associated protein D (SP-D) is a soluble innate immune collectin present on many mucosal surfaces. We recently showed that SP-D suppresses the extrinsic pathway of apoptosis by downregulating caspase-8 activation. However, the effects of SP-D on the intrinsic pathway of apoptosis are not clearly understood. In the intrinsic pathway, cytochrome c is released by mitochondria into the cytoplasm. Oxidation of cytochrome c by cytochrome c oxidase activates the apoptosome and caspase-9 cascade. Both caspase-8- and caspase-9-mediated branches are activated in the intrinsic pathway of apoptosis; however, little is known about the relevance of the caspase-8 pathway in this context. Here we studied the effects of SP-D on different branches of the intrinsic pathway of apoptosis using UV-irradiated Jurkat T-cells. We found that SP-D does not inhibit the caspase-9 branch of apoptosis and the relevance of the caspase-8-related branch became apparent when the caspase-9 pathway was inhibited by blocking cytochrome c oxidase. Under these conditions, SP-D reduces the activation of caspase-8, executioner caspase-3 and exposure of phosphatidylserine (PS) on the membranes of dying cells. By contrast, SP-D increases the formation of nuclear and membrane blebs. Inhibition of caspase-8 confirms the effect of SP-D is unique to the caspase-8 pathway. Overall, SP-D suppresses certain aspects of the intrinsic pathway of apoptosis via reduction of caspase-8 activation and PS flipping while at the same time increasing membrane and nuclear bleb formation. This novel regulatory aspect of SP-D could help to regulate intrinsic pathway of apoptosis to promote effective blebbing and breakdown of dying cells.
MeSH term(s)	Apoptosis/immunology ; Caspase 3/immunology ; Caspase 8/immunology ; Caspase 9/immunology ; Cell Membrane Structures/immunology ; Cytochromes c/immunology ; Humans ; Jurkat Cells ; Nuclear Envelope/immunology ; Pulmonary Surfactant-Associated Protein D/immunology ; Signal Transduction/immunology
Chemical Substances	Pulmonary Surfactant-Associated Protein D ; Cytochromes c (9007-43-6) ; CASP3 protein, human (EC 3.4.22.-) ; CASP8 protein, human (EC 3.4.22.-) ; CASP9 protein, human (EC 3.4.22.-) ; Caspase 3 (EC 3.4.22.-) ; Caspase 8 (EC 3.4.22.-) ; Caspase 9 (EC 3.4.22.-)
Language	English
Publishing date	2017-11-04
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	424427-8
ISSN	1872-9142 ; 0161-5890
ISSN (online)	1872-9142
ISSN	0161-5890
DOI	10.1016/j.molimm.2017.10.016
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Article: Surfactant Protein D Regulates Caspase-8-mediated Cascade of the Intrinsic Pathway of Apoptosis While Promoting Bleb Formation

Djiadeu, Pascal / Nicole Farmakovski / Dhia Azzouz / Lakshmi P. Kotra / Neil Sweezey / Nades Palaniyar

Molecular Immunology. 2017,

2017

Abstract	Surfactant-associated protein D (SP-D) is a soluble innate immune collectin present on many mucosal surfaces. We recently showed that SP-D suppresses the extrinsic pathway of apoptosis by downregulating caspase-8 activation. However, the effects of SP-D on the intrinsic pathway of apoptosis are not clearly understood. In the intrinsic pathway, cytochrome c is released by mitochondria into the cytoplasm. Oxidation of cytochrome c by cytochrome c oxidase activates the apoptosome and caspase-9 cascade. Both caspase-8- and caspase-9-mediated branches are activated in the intrinsic pathway of apoptosis; however, little is known about the relevance of the caspase-8 pathway in this context. Here we studied the effects of SP-D on different branches of the intrinsic pathway of apoptosis using UV-irradiated Jurkat T-cells. We found that SP-D does not inhibit the caspase-9 branch of apoptosis and the relevance of the caspase-8-related branch became apparent when the caspase-9 pathway was inhibited by blocking cytochrome c oxidase. Under these conditions, SP-D reduces the activation of caspase-8, executioner caspase-3 and exposure of phosphatidylserine (PS) on the membranes of dying cells. By contrast, SP-D increases the formation of nuclear and membrane blebs. Inhibition of caspase-8 confirms the effect of SP-D is unique to the caspase-8 pathway. Overall, SP-D suppresses certain aspects of the intrinsic pathway of apoptosis via reduction of caspase-8 activation and PS flipping while at the same time increasing membrane and nuclear bleb formation. This novel regulatory aspect of SP-D could help to regulate intrinsic pathway of apoptosis to promote effective blebbing and breakdown of dying cells.
Keywords	T-lymphocytes ; apoptosis ; caspase-3 ; caspase-8 ; caspase-9 ; cytochrome c ; cytochrome-c oxidase ; mitochondria ; mucosa ; oxidation ; phosphatidylserines ; surfactants ; ultraviolet radiation
Language	English
Size	p. .
Publishing place	Elsevier Ltd
Document type	Article
Note	Pre-press version
ZDB-ID	424427-8
ISSN	1872-9142 ; 0161-5890
ISSN (online)	1872-9142
ISSN	0161-5890
DOI	10.1016/j.molimm.2017.10.016
Database	NAL-Catalogue (AGRICOLA)

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Zs.A 166: Show issues

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Article: Validation of the Tunisian versions of Bath Ankylosing Spondylitis Functional Index (BASFI) and Disease Activity Index (BASDAI).

Kchir, Mohamed Montacer / Hamdi, Wafa / Kochbati, Samir / Azzouz, Dhouha / Daoud, Lilia / Saadellaoui, Kaouthar / Ghannouchi, Mohamed Mehdi / Kaffel, Dhia / Ben Hamida, Abdelmajid / Zouari, Béchir

La Tunisie medicale

2009 Volume 87, Issue 8, Page(s) 527–530

Abstract: Background: The Bath Ankylosing Spondylitis Functional Index (BASFI) and the Bath Ankylosing Spondylitis Disease Activity (BASDAI) are the most commonly used instruments to evaluate respectively functioning and disease activity in ankylosing spondylitis ...

Abstract	Background: The Bath Ankylosing Spondylitis Functional Index (BASFI) and the Bath Ankylosing Spondylitis Disease Activity (BASDAI) are the most commonly used instruments to evaluate respectively functioning and disease activity in ankylosing spondylitis (AS). Objective: The aim of this study was to translate, adapt and validate these instruments into the Tunisian language. Methods: The studied population consisted of 68 AS patients (59 males and 9 females). Their mean age was 37.9 years (range: 18-76). The mean disease duration was 13.6 years (range: 1-40). After translation and retranslation the BASFI and BASDAI questionnaires were administrated to the patients and tested for reliability, internal consistency and construct validity. Results: The reproducibility of the indices BASFI and BASFAI was good, the intraclass correlation coefficient for reliability was 0.96 (CCI:0.93-0.97) for the BASFI and 0.93 (CCI:0.90-0.97) for the BASDAI, and the coefficient of internal consistency (Cronbach's alpha) was 0.91 for BASFI and 0.90 for BASDAI. Concerning construct validity, both questionnaires were significantly correlated to each other, to the disease-specific instruments (BASG-s, BASMI, BASRI, ASQoL) and to all domains of the SF-36. Conclusion: The Tunisian versions of the BASFI and the BASDAI preserve the metrological properties of the original versions and were easy to use for the assessment of disease status in ankylosing spondylitis.
MeSH term(s)	Adolescent ; Adult ; Aged ; Disability Evaluation ; Female ; Humans ; Male ; Middle Aged ; Reproducibility of Results ; Severity of Illness Index ; Spondylitis, Ankylosing/physiopathology ; Tunisia ; Young Adult
Language	English
Publishing date	2009-08
Publishing country	Tunisia
Document type	Journal Article ; Validation Studies
ZDB-ID	128627-4
ISSN	0041-4131
ISSN	0041-4131
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Article ; Online: HLA-B, DR and DQ antigens polymorphism in Tunisian patients with ankylosing spondylitis (a case-control study).

Kchir, Mohamed Montacer / Hamdi, Wafa / Laadhar, Lilia / Kochbati, Samir / Kaffel, Dhia / Saadellaoui, Kaouthar / Lahmar, Houria / Ghannouchi, Mohamed Mehdi / Azzouz, Dhouha / Daoud, Lilia / Ben Hamida, Abdelmajid / Zouari, Béchir / Zitouni, Mondher / Makni, Sondes

Rheumatology international

2009 Volume 30, Issue 7, Page(s) 933–939

Abstract: The objective of the study is to assess the distribution of HLA-B genes, HLA-B27 subtypes, HLA-DRB1 and HLA-DQB1 alleles in patients with ankylosing spondylitis (AS) and in control subjects in the Tunisian population and to compare their distribution ... ...

Abstract	The objective of the study is to assess the distribution of HLA-B genes, HLA-B27 subtypes, HLA-DRB1 and HLA-DQB1 alleles in patients with ankylosing spondylitis (AS) and in control subjects in the Tunisian population and to compare their distribution with that found in other countries. This is a case-control study that included 100 consecutive patients (85 males/15 females) with AS according to the modified New York criteria and 100 control individuals. HLA-B, B27 subtypes and class II (DR and DQ) typing of all subjects was performed by polymerase chain reaction amplification with sequence-specific primers (PCR-SSP). HLA-B27 was found in 62% of patients against 3% in controls (P = 0.0000, OR = 52.6, 15.6 < CI < 166.7). On the other hand, B07 and B51 were significantly decreased in comparison with controls (P = 0.01, OR = 0.3, 0.1 < CI < 0.8 and P = 0.0000, OR = 0.2, 0.1 < CI < 0.4, respectively). Eight B27 subtypes were identified in the AS group, but the most frequent ones were B2702 (32%) and B2705 (24%). Among HLA-DRB1 alleles, a significant increase in DRB111 was found in comparison with controls (P = 0.01, OR = 2.2, 1.2 < CI < 4.5). However, DRB113 had a negative association with AS (P = 0.01, OR = 0.4, 0.2 < CI < 0.8). For HLA-DQB1 alleles, a significant positive association with DQB103 was observed in AS group (P = 0.03, OR = 1.8, 1.0 < CI < 3.4). Multivariate analysis by logistic regression revealed that DRB111 and DQB103 had no direct links with the disease, but were dependent on the presence of HLA-B27. Moreover, B07 and B51 seemed to have independently a negative correlation with AS, but DRB113 seemed to depend on B51. Haplotypes carrying B27 were significantly associated with AS and those carrying B07 or B51 were negatively correlated with the disease. In conclusion, our study confirms that B27 predisposes to AS while B07 and B51 are negatively correlated with the disease.
MeSH term(s)	Adolescent ; Adult ; Aged ; Biomarkers/analysis ; Biomarkers/blood ; Case-Control Studies ; DNA Mutational Analysis ; Female ; Gene Frequency/genetics ; Genetic Markers/genetics ; Genetic Predisposition to Disease/genetics ; Genetic Testing ; Genotype ; HLA-B Antigens/genetics ; HLA-B27 Antigen/genetics ; HLA-DQ Antigens/genetics ; HLA-DQ beta-Chains ; HLA-DR Antigens/genetics ; HLA-DRB1 Chains ; Humans ; Male ; Middle Aged ; Polymorphism, Genetic/genetics ; Predictive Value of Tests ; RNA, Messenger/analysis ; RNA, Messenger/metabolism ; Spondylitis, Ankylosing/blood ; Spondylitis, Ankylosing/genetics ; Spondylitis, Ankylosing/immunology ; Tunisia ; Young Adult
Chemical Substances	Biomarkers ; Genetic Markers ; HLA-B Antigens ; HLA-B27 Antigen ; HLA-DQ Antigens ; HLA-DQ beta-Chains ; HLA-DQB1 antigen ; HLA-DR Antigens ; HLA-DRB1 Chains ; RNA, Messenger
Language	English
Publishing date	2009-08-05
Publishing country	Germany
Document type	Journal Article
ZDB-ID	8286-7
ISSN	1437-160X ; 0172-8172
ISSN (online)	1437-160X
ISSN	0172-8172
DOI	10.1007/s00296-009-1079-0
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