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Article ; Online: 443 COVID19 disease severity influences the expression of markers of durability in memory B cells

Raphael Reyes / Kathleen Clarke / Angelene M. Cantwell / Gabriel Catano / Robin E. Tragus / Thomas F. Patterson / Sebastiaan Bol / Evelien M Bunnik

Journal of Clinical and Translational Science, Vol 6, Pp 87-

2022 Volume 88

Abstract: OBJECTIVES/GOALS: Studies have shown that SARS-CoV-2 specific memory B cells can be maintained at least a year after exposure. However, reports show an altered B cell response during infection in severe COVID-19 cases. This study aims to describe the B ... ...

Abstract	OBJECTIVES/GOALS: Studies have shown that SARS-CoV-2 specific memory B cells can be maintained at least a year after exposure. However, reports show an altered B cell response during infection in severe COVID-19 cases. This study aims to describe the B cell response during COVID-19 convalescence with a focus on signatures that contribute to durable and robust immunity. METHODS/STUDY POPULATION: Our study cohort consisted of individuals who had recovered from non-severe (hospitalized) or severe (hospitalized and requiring invasive mechanical ventilation) COVID-19. In our comparative analysis, samples from both groups were carefully matched to fall within 4-5 weeks post-symptom onset. We also performed a longitudinal analysis of non-severe patients with sampling ending 5 months post-symptom onset. Using high parameter flow cytometry, we characterized the phenotype of memory B cells using 19 distinct cell markers and fluorescently labeled probes to identify B cells reactive with SARS-CoV-2 spike and receptor-binding domain protein. Additionally, serum collected from individuals was used to quantify antibody titers. RESULTS/ANTICIPATED RESULTS: The frequency of spike-specific B cells and serum antibody titers were similar between severe and non-severe groups. However, we observed that individuals recovered from severe COVID-19 have a significantly reduced frequency of spike specific IgG+ memory B cells expressing Tbet and FcRL5 (markers associated with long lived immunity). In the non-severe patients, we observed IgG+Tbet+ B cells targeting the spike protein peak at 2-3 weeks post-symptom onset, decrease by almost fifty percent 4-5 weeks post-symptom onset, and return to baseline 5 months post-symptom onset. Our study also validated previous findings of a short-lived primary response of IgM+ B cells targeting the spike protein. DISCUSSION/SIGNIFICANCE: Our findings highlight potential implications for long-term immunity against re-infection or severity of the resulting disease in patients with severe COVID-19. ...
Keywords	Medicine ; R
Subject code	610 ; 616
Language	English
Publishing date	2022-04-01T00:00:00Z
Publisher	Cambridge University Press
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: SARS-CoV-2 spike-specific memory B cells express markers of durable immunity after non-severe COVID-19 but not after severe disease.

Reyes, Raphael A / Clarke, Kathleen / Gonzales, S Jake / Cantwell, Angelene M / Garza, Rolando / Catano, Gabriel / Tragus, Robin E / Patterson, Thomas F / Bol, Sebastiaan / Bunnik, Evelien M

bioRxiv : the preprint server for biology

2021

Abstract: SARS-CoV-2 infection elicits a robust B cell response, resulting in the generation of long-lived plasma cells and memory B cells. Here, we aimed to determine the effect of COVID-19 severity on the memory B cell response and characterize changes in the ... ...

Abstract	SARS-CoV-2 infection elicits a robust B cell response, resulting in the generation of long-lived plasma cells and memory B cells. Here, we aimed to determine the effect of COVID-19 severity on the memory B cell response and characterize changes in the memory B cell compartment between recovery and five months post-symptom onset. Using high-parameter spectral flow cytometry, we analyzed the phenotype of memory B cells with reactivity against the SARS-CoV-2 spike protein or the spike receptor binding domain (RBD) in recovered individuals who had been hospitalized with non-severe (n=8) or severe (n=5) COVID-19. One month after symptom onset, a substantial proportion of spike-specific IgG
Language	English
Publishing date	2021-09-27
Publishing country	United States
Document type	Preprint
DOI	10.1101/2021.09.24.461732
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Kinetic Multi-omic Analysis of Responses to SARS-CoV-2 Infection in a Model of Severe COVID-19.

Cantwell, Angelene M / Singh, Harinder / Platt, Maryann / Yu, Yanbao / Lin, Yi-Han / Ikeno, Yuji / Hubbard, Gene / Xiang, Yan / Gonzalez-Juarbe, Norberto / Dube, Peter H

Journal of virology

2021 Volume 95, Issue 20, Page(s) e0101021

Abstract: The host response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is poorly understood due to a lack of an animal model that recapitulates severe human disease. Here, we report a Syrian hamster model that develops progressive lethal ... ...

Abstract	The host response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is poorly understood due to a lack of an animal model that recapitulates severe human disease. Here, we report a Syrian hamster model that develops progressive lethal pulmonary disease that closely mimics severe coronavirus disease 2019 (COVID-19). We evaluated host responses using a multi-omic, multiorgan approach to define proteome, phosphoproteome, and transcriptome changes. These data revealed both type I and type II interferon-stimulated gene and protein expression along with a progressive increase in chemokines, monocytes, and neutrophil-associated molecules throughout the course of infection that peaked in the later time points correlating with a rapidly developing diffuse alveolar destruction and pneumonia that persisted in the absence of active viral infection. Extrapulmonary proteome and phosphoproteome remodeling was detected in the heart and kidneys following viral infection. Together, our results provide a kinetic overview of multiorgan host responses to severe SARS-CoV-2 infection
MeSH term(s)	Animals ; COVID-19/genetics ; COVID-19/immunology ; COVID-19/metabolism ; COVID-19/virology ; Disease Models, Animal ; Gene Ontology ; Heart/virology ; Immunity, Innate ; Kidney/metabolism ; Kidney/virology ; Lung/immunology ; Lung/metabolism ; Lung/pathology ; Lung/virology ; Male ; Mesocricetus ; Myocardium/metabolism ; Phosphoproteins/metabolism ; Proteome ; Proteomics ; SARS-CoV-2/genetics ; SARS-CoV-2/physiology ; Severity of Illness Index ; Transcriptome ; Viral Load
Chemical Substances	Phosphoproteins ; Proteome
Language	English
Publishing date	2021-07-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; 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.01010-21
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Article ; Online: SARS-CoV-2 spike-specific memory B cells express higher levels of T-bet and FcRL5 after non-severe COVID-19 as compared to severe disease.

Raphael A Reyes / Kathleen Clarke / S Jake Gonzales / Angelene M Cantwell / Rolando Garza / Gabriel Catano / Robin E Tragus / Thomas F Patterson / Sebastiaan Bol / Evelien M Bunnik

PLoS ONE, Vol 16, Iss 12, p e

2021 Volume 0261656

Abstract	SARS-CoV-2 infection elicits a robust B cell response, resulting in the generation of long-lived plasma cells and memory B cells. Here, we aimed to determine the effect of COVID-19 severity on the memory B cell response and characterize changes in the memory B cell compartment between recovery and five months post-symptom onset. Using high-parameter spectral flow cytometry, we analyzed the phenotype of memory B cells with reactivity against the SARS-CoV-2 spike protein or the spike receptor binding domain (RBD) in recovered individuals who had been hospitalized with non-severe (n = 8) or severe (n = 5) COVID-19. One month after symptom onset, a substantial proportion of spike-specific IgG+ B cells showed an activated phenotype. In individuals who experienced non-severe disease, spike-specific IgG+ B cells showed increased expression of markers associated with durable B cell memory, including T-bet and FcRL5, as compared to individuals who experienced severe disease. While the frequency of T-bet+ spike-specific IgG+ B cells differed between the two groups, these cells predominantly showed an activated switched memory B cell phenotype in both groups. Five months post-symptom onset, the majority of spike-specific memory B cells had a resting phenotype and the percentage of spike-specific T-bet+ IgG+ memory B cells decreased to baseline levels. Collectively, our results highlight subtle differences in the B cells response after non-severe and severe COVID-19 and suggest that the memory B cell response elicited during non-severe COVID-19 may be of higher quality than the response after severe disease.
Keywords	Medicine ; R ; Science ; Q
Subject code	612 ; 610
Language	English
Publishing date	2021-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: SARS-CoV-2 spike-specific memory B cells express higher levels of T-bet and FcRL5 after non-severe COVID-19 as compared to severe disease.

Reyes, Raphael A / Clarke, Kathleen / Gonzales, S Jake / Cantwell, Angelene M / Garza, Rolando / Catano, Gabriel / Tragus, Robin E / Patterson, Thomas F / Bol, Sebastiaan / Bunnik, Evelien M

PloS one

2021 Volume 16, Issue 12, Page(s) e0261656

Abstract	SARS-CoV-2 infection elicits a robust B cell response, resulting in the generation of long-lived plasma cells and memory B cells. Here, we aimed to determine the effect of COVID-19 severity on the memory B cell response and characterize changes in the memory B cell compartment between recovery and five months post-symptom onset. Using high-parameter spectral flow cytometry, we analyzed the phenotype of memory B cells with reactivity against the SARS-CoV-2 spike protein or the spike receptor binding domain (RBD) in recovered individuals who had been hospitalized with non-severe (n = 8) or severe (n = 5) COVID-19. One month after symptom onset, a substantial proportion of spike-specific IgG+ B cells showed an activated phenotype. In individuals who experienced non-severe disease, spike-specific IgG+ B cells showed increased expression of markers associated with durable B cell memory, including T-bet and FcRL5, as compared to individuals who experienced severe disease. While the frequency of T-bet+ spike-specific IgG+ B cells differed between the two groups, these cells predominantly showed an activated switched memory B cell phenotype in both groups. Five months post-symptom onset, the majority of spike-specific memory B cells had a resting phenotype and the percentage of spike-specific T-bet+ IgG+ memory B cells decreased to baseline levels. Collectively, our results highlight subtle differences in the B cells response after non-severe and severe COVID-19 and suggest that the memory B cell response elicited during non-severe COVID-19 may be of higher quality than the response after severe disease.
MeSH term(s)	Adult ; Aged ; Antibodies, Viral/blood ; B-Lymphocytes/metabolism ; Biomarkers/analysis ; COVID-19/immunology ; COVID-19/metabolism ; Female ; Flow Cytometry/methods ; Hospitalization/trends ; Humans ; Immunoglobulin G/blood ; Immunologic Memory ; Male ; Memory B Cells/immunology ; Memory B Cells/metabolism ; Middle Aged ; Receptors, Fc/blood ; Receptors, Fc/genetics ; Receptors, Fc/metabolism ; SARS-CoV-2/immunology ; SARS-CoV-2/pathogenicity ; Severity of Illness Index ; Spike Glycoprotein, Coronavirus/immunology ; T-Box Domain Proteins/blood ; T-Box Domain Proteins/metabolism
Chemical Substances	Antibodies, Viral ; Biomarkers ; FCRL5 protein, human ; Immunoglobulin G ; Receptors, Fc ; Spike Glycoprotein, Coronavirus ; T-Box Domain Proteins ; T-box transcription factor TBX21 ; spike protein, SARS-CoV-2
Language	English
Publishing date	2021-12-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0261656
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: SARS-CoV-2 spike-specific memory B cells express markers of durable immunity after non-severe COVID-19 but not after severe disease

Reyes, Raphael / Clarke, Kathleen / Gonzales, S. Jake / Cantwell, Angelene M. / Garza, Rolando / Catano, Gabriel / Tragus, Robin E. / Patterson, Thomas F. / Bol, Sebastiaan / Bunnik, Evelien M

bioRxiv

Abstract	SARS-CoV-2 infection elicits a robust B cell response, resulting in the generation of long-lived plasma cells and memory B cells. Here, we aimed to determine the effect of COVID-19 severity on the memory B cell response and characterize changes in the memory B cell compartment between recovery and five months post-symptom onset. Using high-parameter spectral flow cytometry, we analyzed the phenotype of memory B cells with reactivity against the SARS-CoV-2 spike protein or the spike receptor binding domain (RBD) in recovered individuals who had been hospitalized with non-severe (n=8) or severe (n=5) COVID-19. One month after symptom onset, a substantial proportion of spike-specific IgG+ B cells showed an activated phenotype. In individuals who experienced non-severe disease, spike-specific IgG+ B cells showed increased expression of markers associated with durable B cell memory, including T-bet, FcRL5, and CD11c, which was not observed after severe disease. Five months post-symptom onset, the majority of spike-specific memory B cells had a resting phenotype and the percentage of spike-specific T-bet+ IgG+ memory B cells decreased to baseline levels. Collectively, our results suggest that the memory B cell response elicited during non-severe COVID-19 may be of higher quality than the response after severe disease.
Keywords	covid19
Language	English
Publishing date	2021-09-27
Publisher	Cold Spring Harbor Laboratory
Document type	Article ; Online
DOI	10.1101/2021.09.24.461732
Database	COVID19

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Article ; Online: YopH inhibits early pro-inflammatory cytokine responses during plague pneumonia.

Cantwell, Angelene M / Bubeck, Sarah S / Dube, Peter H

BMC immunology

2010 Volume 11, Page(s) 29

Abstract: Background: Yersinia pestis is the causative agent of pneumonic plague; recently, we and others reported that during the first 24-36 hours after pulmonary infection with Y. pestis pro-inflammatory cytokine expression is undetectable in lung tissues.: ... ...

Abstract	Background: Yersinia pestis is the causative agent of pneumonic plague; recently, we and others reported that during the first 24-36 hours after pulmonary infection with Y. pestis pro-inflammatory cytokine expression is undetectable in lung tissues. Results: Here, we report that, intranasal infection of mice with CO92 delta yopH mutant results in an early pro-inflammatory response in the lungs characterized by an increase in the pro-inflammatory cytokines Tumor Necrosis Factor-alpha and Interleukin one-beta 24 hours post-infection. CO92 delta yopH colonizes the lung but does not disseminate to the liver or spleen and is cleared from the host within 72 hours post-infection. This is different from what is observed in a wild-type CO92 infection, where pro-inflammatory cytokine expression and immune cell infiltration into the lungs is not detectable until 36-48 h post-infection. CO92 rapidly disseminates to the liver and spleen resulting in high bacterial burdens in these tissues ultimately cumulating in death 72-94 h post-infection. Mice deficient in TNF-alpha are more susceptible to CO92 delta yopH infection with 40% of the mice succumbing to infection. Conclusions: Altogether, our results suggest that YopH can inhibit an early pro-inflammatory response in the lungs of mice and that this is an important step in the pathogenesis of infection.
MeSH term(s)	Administration, Intranasal ; Animals ; Antibodies/immunology ; Bacterial Outer Membrane Proteins/immunology ; Bronchoalveolar Lavage Fluid/microbiology ; Cytokines/immunology ; Disease Models, Animal ; Female ; Inflammation Mediators/immunology ; Interleukin-1beta/biosynthesis ; Lung/immunology ; Lung/microbiology ; Lung/pathology ; Mice ; Mutation/genetics ; Plague/immunology ; Plague/microbiology ; Plague/pathology ; Protein Tyrosine Phosphatases/deficiency ; Protein Tyrosine Phosphatases/immunology ; Tumor Necrosis Factor-alpha/biosynthesis ; Tumor Necrosis Factor-alpha/deficiency ; Virulence/immunology ; Yersinia pestis/enzymology ; Yersinia pestis/immunology ; Yersinia pestis/pathogenicity
Chemical Substances	Antibodies ; Bacterial Outer Membrane Proteins ; Cytokines ; Inflammation Mediators ; Interleukin-1beta ; Tumor Necrosis Factor-alpha ; Protein Tyrosine Phosphatases (EC 3.1.3.48) ; yopH protein, Yersinia (EC 3.1.3.48)
Language	English
Publishing date	2010-06-16
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	1471-2172
ISSN (online)	1471-2172
DOI	10.1186/1471-2172-11-29
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: YopH inhibits early pro-inflammatory cytokine responses during plague pneumonia

Bubeck Sarah S / Cantwell Angelene M / Dube Peter H

BMC Immunology, Vol 11, Iss 1, p

2010 Volume 29

Abstract: Abstract Background Yersinia pestis is the causative agent of pneumonic plague; recently, we and others reported that during the first 24-36 hours after pulmonary infection with Y. pestis pro-inflammatory cytokine expression is undetectable in lung ... ...

Abstract	Abstract Background Yersinia pestis is the causative agent of pneumonic plague; recently, we and others reported that during the first 24-36 hours after pulmonary infection with Y. pestis pro-inflammatory cytokine expression is undetectable in lung tissues. Results Here, we report that, intranasal infection of mice with CO92 delta yopH mutant results in an early pro-inflammatory response in the lungs characterized by an increase in the pro-inflammatory cytokines Tumor Necrosis Factor-alpha and Interleukin one-beta 24 hours post-infection. CO92 delta yopH colonizes the lung but does not disseminate to the liver or spleen and is cleared from the host within 72 hours post-infection. This is different from what is observed in a wild-type CO92 infection, where pro-inflammatory cytokine expression and immune cell infiltration into the lungs is not detectable until 36-48 h post-infection. CO92 rapidly disseminates to the liver and spleen resulting in high bacterial burdens in these tissues ultimately cumulating in death 72-94 h post-infection. Mice deficient in TNF-alpha are more susceptible to CO92 delta yopH infection with 40% of the mice succumbing to infection. Conclusions Altogether, our results suggest that YopH can inhibit an early pro-inflammatory response in the lungs of mice and that this is an important step in the pathogenesis of infection.
Keywords	Immunologic diseases. Allergy ; RC581-607 ; Specialties of internal medicine ; RC581-951 ; Internal medicine ; RC31-1245 ; Medicine ; R ; DOAJ:Allergy and Immunology ; DOAJ:Medicine (General) ; DOAJ:Health Sciences
Subject code	570
Language	English
Publishing date	2010-06-01T00:00:00Z
Publisher	BioMed Central
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Delayed inflammatory response to primary pneumonic plague occurs in both outbred and inbred mice.

Bubeck, Sarah S / Cantwell, Angelene M / Dube, Peter H

Infection and immunity

2007 Volume 75, Issue 2, Page(s) 697–705

Abstract: Yersinia pestis is the causative agent of plague, a disease that can manifest as either bubonic or pneumonic plague. An interesting feature of plague is that it is a rapidly progressive disease, suggesting that Y. pestis either evades and/or suppresses ... ...

Abstract	Yersinia pestis is the causative agent of plague, a disease that can manifest as either bubonic or pneumonic plague. An interesting feature of plague is that it is a rapidly progressive disease, suggesting that Y. pestis either evades and/or suppresses the innate immune response to infection. Therefore, the early host response during the course of primary pneumonic plague was investigated in two mouse strains, the outbred strain CD1 and the inbred strain C57BL/6. A comparative analysis of the course of disease in these two strains of mice indicated that they are susceptible to intranasal Y. pestis CO92 infection and have similar 50% lethal doses and kinetics of infection with respect to colonization of the lung, liver, and spleen. Significantly, in both strains of mice, robust neutrophil recruitment to the lungs was not observed until 48 h after infection, suggesting that there was a delay in inflammatory cell recruitment to the site of infection. In addition, proinflammatory cytokines (interleukin-6 [IL-6], tumor necrosis factor alpha, gamma interferon, IL-12p70, monocyte chemoattractant protein 1) and chemokines (KC, MIP-2) in the bronchoalveolar lavage fluids were not readily detected until 48 h after infection, which coincided with the increase in polymorphonuclear leukocyte (PMN) recruitment to the lungs. In comparison, CD1 mice with gram-negative pneumonia caused by Klebsiella pneumoniae exhibited strong inflammatory responses early in infection, with PMNs comprising the majority of the cells in the bronchoalveolar lavage fluid 24 h postinfection, indicating that PMN recruitment to the lungs could occur earlier in this infection than in Y. pestis infection. Together, our results indicate that there is a delay in the recruitment of neutrophils to the lungs in the mouse model of primary plague pneumonia that correlates with delayed expression of proinflammatory cytokines and chemokines in both outbred and inbred mice.
MeSH term(s)	Animals ; Bronchoalveolar Lavage Fluid/cytology ; Bronchoalveolar Lavage Fluid/immunology ; Chemokines/metabolism ; Cytokines/metabolism ; Disease Models, Animal ; Female ; Histocytochemistry ; Klebsiella Infections/immunology ; Klebsiella pneumoniae/immunology ; Lethal Dose 50 ; Liver/microbiology ; Lung/immunology ; Lung/microbiology ; Mice ; Mice, Inbred C57BL ; Neutrophil Infiltration ; Neutrophils/immunology ; Plague/immunology ; Plague/microbiology ; Plague/pathology ; Spleen/microbiology ; Time Factors ; Yersinia pestis/growth & development ; Yersinia pestis/immunology
Chemical Substances	Chemokines ; Cytokines
Language	English
Publishing date	2007-02
Publishing country	United States
Document type	Comparative Study ; Journal Article
ZDB-ID	218698-6
ISSN	1098-5522 ; 0019-9567
ISSN (online)	1098-5522
ISSN	0019-9567
DOI	10.1128/IAI.00403-06
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: An age-old paradigm challenged: old baboons generate vigorous humoral immune responses to LcrV, a plague antigen.

Stacy, Sue / Pasquali, Amanda / Sexton, Valerie L / Cantwell, Angelene M / Kraig, Ellen / Dube, Peter H

Journal of immunology (Baltimore, Md. : 1950)

2008 Volume 181, Issue 1, Page(s) 109–115

Abstract: Immune senescence in the elderly results in decreased immunity with a concomitant increase in susceptibility to infection and diminished efficacy of vaccination. Nonhuman primate models have proven critical for testing of vaccines and therapeutics in the ...

Abstract	Immune senescence in the elderly results in decreased immunity with a concomitant increase in susceptibility to infection and diminished efficacy of vaccination. Nonhuman primate models have proven critical for testing of vaccines and therapeutics in the general population, but a model using old animals has not been established. Toward that end, immunity to LcrV, a protective Ag from Yersinia pestis, was tested in young and old baboons. Surprisingly, there was no age-associated loss in immune competence; LcrV elicited high-titer, protective Ab responses in the older individuals. The primary responses in the younger baboons were lower, but they did show boosting upon secondary immunization to the levels achieved in the old animals. The LcrV Ag was also tested in mice and, as expected, age-associated loss of immunity was seen; older animals responded with lower-titer Abs and, as a result, were more susceptible to Yersinia challenge. Thus, although age-related loss in immune function has been observed in humans, rodents, and some nonhuman primates, baboons appear to be unusual; they age without losing immune competence.
MeSH term(s)	Aging/immunology ; Animals ; Antibodies/immunology ; Antibody Formation/immunology ; Antigens, Bacterial/immunology ; Chimerism ; Mice ; Papio/immunology ; Plague Vaccine/immunology ; Pore Forming Cytotoxic Proteins/immunology ; Yersinia pestis/immunology
Chemical Substances	Antibodies ; Antigens, Bacterial ; LcrV protein, Yersinia ; Plague Vaccine ; Pore Forming Cytotoxic Proteins
Language	English
Publishing date	2008-06-17
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.181.1.109
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