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  1. Article ; Online: Epicutaneous immunization with TNP-Ig antigen induces CD11c

    Majewska-Szczepanik, Monika / Strzępa, Anna / Marcińska, Katarzyna / Szczepanik, Marian

    International immunopharmacology

    2023  Volume 119, Page(s) 110281

    Abstract: The contact hypersensitivity response (CHS) is a mouse model of allergic contact dermatitis in humans. The reaction is classified as type IV hypersensitivity and underlies many autoimmune disorders. Experiments employing the CHS model in wild-type mice ... ...

    Abstract The contact hypersensitivity response (CHS) is a mouse model of allergic contact dermatitis in humans. The reaction is classified as type IV hypersensitivity and underlies many autoimmune disorders. Experiments employing the CHS model in wild-type mice showed that the protein antigen applied to the skin in the form of a gauze patch one week before the induction of Th1-dependent CHS was an effective strategy to reduce the inflammatory response in the skin. The approach of epicutaneous (EC) immunization also effectively suppressed the inflammatory response in various mouse models of autoimmune diseases. To evaluate the potential of EC immunization to suppress T cell-dependent immune response in humans, we used HLA-DR4 tg mice, which express the human DRB1*0401 allele and lack all endogenous mouse MHC class II genes. Our data show that EC immunization with TNP-conjugated protein antigen followed by induction of CHS to trinitrochlorobenzene (TNCB), effectively suppressed the CHS response as described by ear swelling, MPO activity in ear extracts, and the number of TCRβ
    MeSH term(s) Mice ; Humans ; Animals ; Mice, Transgenic ; HLA-DR4 Antigen/genetics ; Interleukin-10 ; Immunization ; Antigens ; Dermatitis, Allergic Contact/therapy ; Dendritic Cells
    Chemical Substances HLA-DR4 Antigen ; Interleukin-10 (130068-27-8) ; Antigens
    Language English
    Publishing date 2023-05-06
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 2043785-7
    ISSN 1878-1705 ; 1567-5769
    ISSN (online) 1878-1705
    ISSN 1567-5769
    DOI 10.1016/j.intimp.2023.110281
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  2. Article: Perinatal treatment of parents with the broad-spectrum antibiotic enrofloxacin aggravates contact sensitivity in adult offspring mice.

    Kowalczyk, Paulina / Strzępa, Anna / Szczepanik, Marian

    Pharmacological reports : PR

    2021  Volume 73, Issue 2, Page(s) 664–671

    Abstract: Background: Antibiotics, while eliminating pathogens, also partially deplete commensal bacteria. Antibiotic-induced dysbiosis may contribute to the observed rise in "immune-mediated" diseases, including autoimmunity and allergy. The aim of this study is ...

    Abstract Background: Antibiotics, while eliminating pathogens, also partially deplete commensal bacteria. Antibiotic-induced dysbiosis may contribute to the observed rise in "immune-mediated" diseases, including autoimmunity and allergy. The aim of this study is to investigate the impact of perinatal antibiotic treatment on T cell-mediated immune response in adult mice.
    Methods: Oral treatment with broad-spectrum antibiotic enrofloxacin during gestation and breastfeeding or breastfeeding or gestation alone was used to evaluate whether antibiotic exposure early in life could modulate contact sensitivity (CS) in adult mice.
    Results: Here, we demonstrated that enrofloxacin treatment during gestation and breastfeeding, but not during pregnancy or breastfeeding alone, aggravated CS reaction in adult mice measured by ear swelling. These data correlate with increased myeloperoxidase (MPO) activity in the ear extracts and elevated production of IL-6 and IL-17A by auricular lymph node cells (ELNC) and was not influenced by food consumption and body weight. In each dosing regimen, enrofloxacin treatment reduced the relative abundance of Enterococcus spp. but did not influence the relative abundances of Lactobacillus, Clostridium cluster XIVa, XIVab, I, Bacteroidetes, and segmented filamentous bacteria (SFB). However, prolonged enrofloxacin-treatment during both gestation and breastfeeding decreased the relative abundance of Clostridium cluster IV.
    Conclusion: These data show that long-term perinatal enrofloxacin treatment induces intestinal dysbiosis, characterized by decreased levels of anti-inflammatory Clostridium cluster IV, and alters T cell-dependent immune responses, enhancing CS reaction in adult mice.
    MeSH term(s) Administration, Oral ; Animals ; Anti-Bacterial Agents/administration & dosage ; Anti-Bacterial Agents/toxicity ; Clostridium/isolation & purification ; Dermatitis, Contact/etiology ; Dermatitis, Contact/immunology ; Dysbiosis/etiology ; Dysbiosis/immunology ; Enrofloxacin/administration & dosage ; Enrofloxacin/toxicity ; Female ; Lactation ; Male ; Mice ; Mice, Inbred BALB C ; Pregnancy ; Prenatal Exposure Delayed Effects/etiology ; Prenatal Exposure Delayed Effects/immunology ; T-Lymphocytes/immunology
    Chemical Substances Anti-Bacterial Agents ; Enrofloxacin (3DX3XEK1BN)
    Language English
    Publishing date 2021-01-22
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2186248-5
    ISSN 1734-1140
    ISSN 1734-1140
    DOI 10.1007/s43440-021-00217-3
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  3. Article ; Online: Diet-induced obesity aggravates NK cell-mediated contact hypersensitivity reaction in Rag1

    Kowalczyk, Paulina / Majewska-Szczepanik, Monika / Strzępa, Anna / Biała, Dominika / Szczepanik, Marian

    Contact dermatitis

    2021  Volume 85, Issue 3, Page(s) 307–316

    Abstract: Background: Previous studies showed that natural killer (NK) cells mediate contact hypersensitivity (CHS) reaction. Many reports are showing that obesity promotes several inflammatory diseases. It was shown that diet-induced obesity (DIO) aggravates ... ...

    Abstract Background: Previous studies showed that natural killer (NK) cells mediate contact hypersensitivity (CHS) reaction. Many reports are showing that obesity promotes several inflammatory diseases. It was shown that diet-induced obesity (DIO) aggravates classical T cell-mediated CHS in mice.
    Objectives: To determine whether the high-fat diet (HFD)-induced obesity modulates antigen-specific NK cell-mediated response.
    Methods: We evaluated the effect of DIO on NK cell-mediated CHS reaction using a model of dinitrofluorobenzene (DNFB)-induced CHS in Rag1
    Results: Rag1
    Conclusions: In summary, current results suggest that the DIO significantly modulates the local and systemic inflammatory response, contributing to exacerbation of the CHS response mediated by liver NK cells.
    MeSH term(s) Adiponectin/metabolism ; Animals ; Cells, Cultured ; Dermatitis, Allergic Contact/complications ; Dermatitis, Allergic Contact/immunology ; Diet, High-Fat/adverse effects ; Disease Models, Animal ; Flow Cytometry ; Interferon-gamma/metabolism ; Interleukin-12/metabolism ; Killer Cells, Natural/immunology ; Leukocytes, Mononuclear/metabolism ; Liver/metabolism ; Male ; Mice, Inbred C57BL ; Mice, Knockout ; Obesity/complications ; Obesity/immunology ; Recombinant Proteins/metabolism ; Mice
    Chemical Substances Adiponectin ; Recombinant Proteins ; interferon gamma-4A ; Interleukin-12 (187348-17-0) ; Interferon-gamma (82115-62-6)
    Language English
    Publishing date 2021-05-11
    Publishing country England
    Document type Journal Article
    ZDB-ID 193121-0
    ISSN 1600-0536 ; 0105-1873
    ISSN (online) 1600-0536
    ISSN 0105-1873
    DOI 10.1111/cod.13871
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  4. Article ; Online: Obesity aggravates contact hypersensitivity reaction in mice.

    Majewska-Szczepanik, Monika / Kowalczyk, Paulina / Marcińska, Katarzyna / Strzępa, Anna / Lis, Grzegorz J / Wong, F Susan / Szczepanik, Marian / Wen, Li

    Contact dermatitis

    2022  Volume 87, Issue 1, Page(s) 28–39

    Abstract: Background: Obesity is associated with chronic, low-grade inflammation in tissues and predisposes to various complications, including inflammatory skin diseases. However, the link between obesity and contact hypersensitivity (CHS) is not fully ... ...

    Abstract Background: Obesity is associated with chronic, low-grade inflammation in tissues and predisposes to various complications, including inflammatory skin diseases. However, the link between obesity and contact hypersensitivity (CHS) is not fully understood.
    Objectives: We sought to determine the influence of obesity on T helper 1 (Th1)-mediated CHS.
    Methods: The activity/phenotype/cytokine profile of the immune cells was tested in vivo and in vitro. Using quantitative polymerase chain reaction (qPCR) and fecal microbiota transplantation (FMT), we tested the role of a high-fat diet (HFD)-induced gut microbiota (GM) dysbiosis in increasing the effects of CHS.
    Results: Exacerbated CHS correlates with an increased inflammation-inducing GM in obese mice. We showed a proinflammatory milieu in the subcutaneous adipose tissue of obese mice, accompanied by proinflammatory CD4+ T cells and dendritic cells in skin draining lymph nodes and spleen. Obese interleukin (IL)-17A-/-B6 mice are protected from CHS aggravation, suggesting the importance of IL-17A in CHS aggravation in obesity.
    Conclusions: Obesity creates a milieu that induces more potent CHS-effector cells but does not have effects on already activated CHS-effector cells. IL-17A is essential for the pathogenesis of enhanced CHS during obesity. Our study provides novel knowledge about antigen-specific responses in obesity, which may help with the improvement of existing treatment and/or in designing novel treatment for obesity-associated skin disorders.
    MeSH term(s) Animals ; CD4-Positive T-Lymphocytes ; Dermatitis, Allergic Contact ; Humans ; Inflammation ; Interleukin-17 ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Obesity
    Chemical Substances Interleukin-17
    Language English
    Publishing date 2022-03-18
    Publishing country England
    Document type Journal Article
    ZDB-ID 193121-0
    ISSN 1600-0536 ; 0105-1873
    ISSN (online) 1600-0536
    ISSN 0105-1873
    DOI 10.1111/cod.14088
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  5. Article ; Online: Oral treatment with enrofloxacin creates anti-inflammatory environment that supports induction of tolerogenic dendritic cells.

    Strzępa, Anna / Marcińska, Katarzyna / Majewska-Szczepanik, Monika / Szczepanik, Marian

    International immunopharmacology

    2019  Volume 77, Page(s) 105966

    Abstract: Background: Oral enrofloxacin treatment altered the gut microbiome promoting anti-inflammatory bacteria. The dysbiosis promotes regulatory cell induction in the intestines and in the periphery, which suppresses contact sensitivity. Bacterial-derived ... ...

    Abstract Background: Oral enrofloxacin treatment altered the gut microbiome promoting anti-inflammatory bacteria. The dysbiosis promotes regulatory cell induction in the intestines and in the periphery, which suppresses contact sensitivity. Bacterial-derived signals promote regulatory cell induction both directly and indirectly by influencing the phenotype of dendritic cells (DC).
    Methods: Oral treatment with broad-spectrum antibiotic enrofloxacin was used to evaluate how gut flora perturbation shapes the immune response in the gut and the periphery.
    Results: Enrofloxacin-induced dysbiosis creates an anti-inflammatory environment characterized by increased IL-10 concentration in the gut lumen and tissues. The production of IFN-γ and IL-17A did not change. Oral enrofloxacin treatment skewed the profile of the immune response towards an anti-inflammatory phenotype locally in small intestinal Peyer's Patches (PP) and systematically in the spleen (SPL). Enrofloxacin administration changed immune response in PP by increasing TGF-β secretion from an increased percentage of TGF-β-producing. In the SPL, enrofloxacin treatment increased the secretion of TGF-β and IL-10 and decreased the secretion of IL-17A and IFN-γ. The shift in cytokine profile correlated with a higher percentage of latency-associated peptide and IL-10-producing cells and a decreased percentage of IFN-γ-producing T cells. This anti-inflammatory immune response in the PP and SPL promoted a higher frequency of tolerogenic DC.
    Conclusion: Our data indicate that two-week enrofloxacin treatment induces dysbiosis, skews immune response towards an anti-inflammatory phenotype, and elevates secretion of TGF-β and IL-10 in the intestines and periphery. Additionally, we observed higher frequencies of tolerogenic DC, characterized by CD11b and IL-10 expression, which are known inducers of Treg cells.
    MeSH term(s) Administration, Oral ; Animals ; Anti-Inflammatory Agents/pharmacology ; Dendritic Cells/drug effects ; Dendritic Cells/metabolism ; Enrofloxacin/pharmacology ; Gastrointestinal Microbiome/drug effects ; Immune Tolerance/drug effects ; Interferon-gamma/metabolism ; Interleukin-10/metabolism ; Interleukin-17/metabolism ; Mice ; Mice, Inbred C57BL ; Peyer's Patches/metabolism ; Spleen/drug effects ; Spleen/metabolism ; T-Lymphocytes, Regulatory/drug effects ; T-Lymphocytes, Regulatory/metabolism ; Transforming Growth Factor beta/metabolism
    Chemical Substances Anti-Inflammatory Agents ; Interleukin-17 ; Transforming Growth Factor beta ; Interleukin-10 (130068-27-8) ; Enrofloxacin (3DX3XEK1BN) ; Interferon-gamma (82115-62-6)
    Language English
    Publishing date 2019-10-31
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 2043785-7
    ISSN 1878-1705 ; 1567-5769
    ISSN (online) 1878-1705
    ISSN 1567-5769
    DOI 10.1016/j.intimp.2019.105966
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  6. Article ; Online: Effect of uterine microbiota on female and offspring health

    Barbara Macura / Monika Majewska-Szczepanik / Anna Strzępa / Marian Szczepanik

    Medycyna Ogólna i Nauki o Zdrowiu, Vol 26, Iss 3, Pp 230-

    2020  Volume 239

    Abstract: Introduction It is well known that the microbiota of the human body is important for human health. The latest technological advances in molecular biology not only confirm the presence of microbial communities in the digestive, respiratory and urinary ... ...

    Abstract Introduction It is well known that the microbiota of the human body is important for human health. The latest technological advances in molecular biology not only confirm the presence of microbial communities in the digestive, respiratory and urinary tracts, but have also led to the detection of the presence of microbiota in niches, previously considered as sterile, for example, in the uterus. Objective In this review we attempt to define the composition of uterine microbiota and its physiological role in the female genital tract. Moreover, we present possible consequences of changes in uterine microbiota composition on the development of gynaecologic disorders. State of knowledge Recent findings suggest the presence of bacteria in amniotic fluid, the umbilical cord blood and in the placenta. This data imply the influence of the uterine microbiota on reproductive and obstetric outcomes, as well as on foetal development and health status. The state of uterine microbiota can influence the efficiency of assisted reproductive technology. Some evidence suggesting a relationship between prenatal microbiota exposure and increased predisposition to some diseases in adulthood is particularly important. Conclusions The influence of the uterine microbiota on fertility disorders, foetus development and newborn health is an important direction of research. In the future, the status of uterine microbiota should play an important role in everyday clinical practice.
    Keywords pregnancy ; microbiota ; uterus ; Medicine (General) ; R5-920
    Language English
    Publishing date 2020-09-01T00:00:00Z
    Publisher Institute of Rural Health
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  7. Article ; Online: Antibiotics and autoimmune and allergy diseases: Causative factor or treatment?

    Strzępa, Anna / Lobo, Francis M / Majewska-Szczepanik, Monika / Szczepanik, Marian

    International immunopharmacology

    2018  Volume 65, Page(s) 328–341

    Abstract: The newborn infant emerges from an almost sterile environment into a world of bacteria. Bacteria colonize the infant's skin, lungs, and, of most importance, the gut. The process of bacterial colonization is coordinated, and each body niche acquires a ... ...

    Abstract The newborn infant emerges from an almost sterile environment into a world of bacteria. Bacteria colonize the infant's skin, lungs, and, of most importance, the gut. The process of bacterial colonization is coordinated, and each body niche acquires a unique composition of bacteria. In the gut, most bacteria belong to the Firmicutes and Bacteroidetes phyla, while Actinobacteria and Proteobacteria are far less abundant. Some of these bacteria possess strong immunoregulatory properties. Bacterial colonization is essential to skew the newborn's immune response away from the allergy-favoring Type-2 response towards a Type-1 immune response, which is essential for pathogen elimination. Imbalance between Type 1 and Type 2 responses, however, can promote autoimmunity. In addition, the microbiota shapes immune responses in adults. Autoimmune and allergic diseases are commonly associated with an altered composition of resident bacteria, which is known as dysbiosis. Perhaps the most common cause of disruption and alteration of the bacterial colonization of newborns is the use of antibiotics. It is not known whether the dysbiosis precedes or is the consequence of allergic and autoimmune disorders, and whether antibiotics can be a trigger for these disorders, depending on the type of antibiotic used and the maturity of immune system. In this review, we discuss the development of the microbiota in different body niches and their immunomodulatory potential. We evaluate the impact of antibiotics, both in mice and in humans, on microbial communities and how that may impact the development and manifestation of diseases through all stages of life: the prenatal period, childhood, and adulthood.
    MeSH term(s) Animals ; Anti-Bacterial Agents/therapeutic use ; Autoimmune Diseases/therapy ; Dysbiosis/therapy ; Female ; Gastrointestinal Microbiome/immunology ; Humans ; Hypersensitivity/therapy ; Infant ; Mice ; Pregnancy ; Th1-Th2 Balance
    Chemical Substances Anti-Bacterial Agents
    Language English
    Publishing date 2018-10-22
    Publishing country Netherlands
    Document type Journal Article ; Review
    ZDB-ID 2043785-7
    ISSN 1878-1705 ; 1567-5769
    ISSN (online) 1878-1705
    ISSN 1567-5769
    DOI 10.1016/j.intimp.2018.10.021
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  8. Article ; Online: Wpływ naturalnej flory jelitowej na odpowiedź immunologiczną.

    Strzępa, Anna / Szczepanik, Marian

    Postepy higieny i medycyny doswiadczalnej (Online)

    2013  Volume 67, Page(s) 908–920

    Abstract: Our intestines are habitat for trillions of microorganisms such as bacteria, viruses and eukaryotes, known as microbiota. They are indispensable for our well-being due to their metabolic activities. Microbiota digests complex plant polysaccharides, which ...

    Title translation Influence of natural gut flora on immune response.
    Abstract Our intestines are habitat for trillions of microorganisms such as bacteria, viruses and eukaryotes, known as microbiota. They are indispensable for our well-being due to their metabolic activities. Microbiota digests complex plant polysaccharides, which are normally unprocessed by humans; as well it retrieves other essential nutrients. It is well established that microbiota is crucial for proper development of intestinal as well systemic immune compartments. Recent results indicate that composition of natural gut flora is responsible for shaping of immune response. Alerted bacterial profile, known as dysbiosis precedes development of allergy in children. Many autoimmune conditions are associated with shift in intestinal bacterial profile. Apart of direct association between gut flora and systemic immune compartment little is known about the mechanisms by which microbiota exerts its immunoregulatory function. At the moment several bacterial strains as well some bacterial products were recognized as immunomodulators. This review describes the composition of normal gut flora as well disease-associated microbiota. It deals with unique mechanisms, found in GALT, that favor induction of tolerance towards orally administrated antigens as well discriminate between commensal and pathogens to minimize induction of inflammatory response. Further, the review tries to establish the connection between microbiota and systemic immune response. Finally the factors that modulate the composition of our gut flora are described.
    MeSH term(s) Autoimmune Diseases/immunology ; Autoimmune Diseases/microbiology ; Bacteria/immunology ; Dysbiosis ; Humans ; Hypersensitivity/immunology ; Hypersensitivity/microbiology ; Immune Tolerance/immunology ; Intestines/immunology ; Intestines/microbiology ; Intestines/virology ; Microbiota/physiology ; Viruses/immunology
    Language Polish
    Publishing date 2013-08-29
    Publishing country Poland
    Document type Journal Article ; Review
    ZDB-ID 418865-2
    ISSN 1732-2693 ; 0032-5449
    ISSN (online) 1732-2693
    ISSN 0032-5449
    DOI 10.5604/17322693.1064563
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  9. Article: Corrigendum to "Epicutaneous immunization with protein antigen TNP-Ig and NOD2 ligand muramyl dipeptide (MDP) reverses skin-induced suppression of contact hypersensitivity" [Pharmacol. Rep. 66 (2014) 137-142].

    Majewska-Szczepanik, Monika / Dorożyńska, Iwona / Strzępa, Anna / Szczepanik, Marian

    Pharmacological reports : PR

    2017  Volume 69, Issue 3, Page(s) 587

    Language English
    Publishing date 2017-03-29
    Publishing country Switzerland
    Document type Journal Article ; Published Erratum
    ZDB-ID 2186248-5
    ISSN 1734-1140
    ISSN 1734-1140
    DOI 10.1016/j.pharep.2017.01.017
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  10. Article ; Online: Neutrophil-Derived Myeloperoxidase Facilitates Both the Induction and Elicitation Phases of Contact Hypersensitivity.

    Strzepa, Anna / Gurski, Cody J / Dittel, Landon J / Szczepanik, Marian / Pritchard, Kirkwood A / Dittel, Bonnie N

    Frontiers in immunology

    2021  Volume 11, Page(s) 608871

    Abstract: Background: Allergic contact dermatitis (ACD) is a common skin disorder affecting an estimated 15-20% of the general population. The mouse model of ACD is contact hypersensitivity (CHS), which consists of two phases: induction and elicitation. Although ... ...

    Abstract Background: Allergic contact dermatitis (ACD) is a common skin disorder affecting an estimated 15-20% of the general population. The mouse model of ACD is contact hypersensitivity (CHS), which consists of two phases: induction and elicitation. Although neutrophils are required for both CHS disease phases their mechanisms of action are poorly understood. Neutrophils release myeloperoxidase (MPO) that through oxidation of biomolecules leads to cellular damage.
    Objectives: This study investigated mechanisms whereby MPO contributes to CHS pathogenesis.
    Methods: CHS was induced in mice using oxazolone (OX) as the initiating hapten applied to the skin. After 7 days, CHS was elicited by application of OX to the ear and disease severity was measured by ear thickness and vascular permeability in the ear. The role of MPO in the two phases of CHS was determined utilizing MPO-deficient mice and a specific MPO inhibitor.
    Results: During the CHS induction phase MPO-deficiency lead to a reduction in IL-1β production in the skin and a subsequent reduction in migratory dendritic cells (DC) and effector T cells in the draining lymph node. During the elicitation phase, inhibition of MPO significantly reduced both ear swelling and vascular permeability.
    Conclusion: MPO plays dual roles in CHS pathogenesis. In the initiation phase MPO promotes IL-1β production in the skin and activation of migratory DC that promote effector T cell priming. In the elicitation phase MPO drives vascular permeability contributing to inflammation. These results indicate that MPO it could be a potential therapeutic target for the treatment of ACD in humans.
    MeSH term(s) Animals ; Cell Movement/immunology ; Dendritic Cells/immunology ; Dermatitis, Allergic Contact/immunology ; Dermatitis, Contact/immunology ; Haptens/immunology ; Inflammation/immunology ; Interleukin-1beta/immunology ; Lymph Nodes/immunology ; Mice ; Mice, Inbred C57BL ; Neutrophils/immunology ; Oxazolone/immunology ; Peroxidase/immunology ; Skin/immunology ; T-Lymphocytes/immunology
    Chemical Substances Haptens ; Interleukin-1beta ; Oxazolone (15646-46-5) ; Peroxidase (EC 1.11.1.7)
    Language English
    Publishing date 2021-01-25
    Publishing country Switzerland
    Document type Journal Article ; Research Support, N.I.H., Extramural ; 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.2020.608871
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