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Article ; Online: Memory B cells and plasma cells: The differentiative continuum of humoral immunity.

Cancro, Michael P / Tomayko, Mary M

2021 Volume 303, Issue 1, Page(s) 72–82

Abstract: Immunological memory is a composite of lasting antibody titers maintained by plasma cells in conjunction with memory T and B cells. Memory B cells are a critical reservoir for plasma cell generation in the secondary response. Identification of memory B ... ...

Abstract	Immunological memory is a composite of lasting antibody titers maintained by plasma cells in conjunction with memory T and B cells. Memory B cells are a critical reservoir for plasma cell generation in the secondary response. Identification of memory B cells requires that they be distinguished from naïve, activated, and germinal center precursors and from plasma cells. Memory B cells are heterogeneous in isotype usage, immunoglobulin mutational content, and phenotypic marker expression. Phenotypic subsets of memory B cells are defined by PD-L2, CD80, and CD73 expression in mice, by CD27 and FCRL4 expression in humans and by T-bet in both mice and humans. These subsets display marked functional heterogeneity, including the ability to rapidly differentiate into plasma cells versus seed germinal centers in the secondary response. Memory B cells are located in the spleen, blood, other lymphoid organs, and barrier tissues, and recent evidence indicates that some memory B cells may be dedicated tissue-resident populations. Open questions about memory B cell longevity, renewal and progenitor-successor relationships with plasma cells are discussed.
MeSH term(s)	Animals ; B-Lymphocytes ; Germinal Center ; Immunity, Humoral ; Immunologic Memory ; Mice ; Plasma Cells
Language	English
Publishing date	2021-08-15
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	391796-4
ISSN	1600-065X ; 0105-2896
ISSN (online)	1600-065X
ISSN	0105-2896
DOI	10.1111/imr.13016
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Article ; Online: Editorial: The nose knows.

Cancro, Michael P / Allman, David M

Journal of leukocyte biology

2017 Volume 102, Issue 3, Page(s) 569–571

MeSH term(s)	Dendritic Cells ; Granulocyte-Macrophage Colony-Stimulating Factor/physiology ; Humans ; Immunoglobulin A/physiology ; Nasal Mucosa ; Toll-Like Receptor 5/physiology
Chemical Substances	Immunoglobulin A ; TLR5 protein, human ; Toll-Like Receptor 5 ; Granulocyte-Macrophage Colony-Stimulating Factor (83869-56-1)
Language	English
Publishing date	2017-08-08
Publishing country	United States
Document type	Editorial ; Comment
ZDB-ID	605722-6
ISSN	1938-3673 ; 0741-5400
ISSN (online)	1938-3673
ISSN	0741-5400
DOI	10.1189/jlb.3CE0517-204R
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Article: The BLyS/BAFF family of ligands and receptors: key targets in the therapy and understanding of autoimmunity.

Cancro, M P

Annals of the rheumatic diseases

2006 Volume 65 Suppl 3, Page(s) iii34–6

Abstract: The B lymphocyte stimulator (BLyS; also termed BAFF) family of ligands and receptors plays a central role in B lymphocyte development, selection, and homoeostasis. Members of this family can independently influence different B cell subsets, because the ... ...

Abstract	The B lymphocyte stimulator (BLyS; also termed BAFF) family of ligands and receptors plays a central role in B lymphocyte development, selection, and homoeostasis. Members of this family can independently influence different B cell subsets, because the interactions between the two ligands and three receptors vary, and the receptors themselves are differentially expressed among developing, naive, and antigen experienced B cell subsets. These properties prompt careful assessment of how ablative therapies may influence the behaviour of upstream or downstream B lineage populations, as well as how the implementation and expectations of therapeutics targeting BLyS family members must be guided by knowledge of the B cell subsets contributing to pathogenesis.
MeSH term(s)	Animals ; Autoimmune Diseases/immunology ; Autoimmune Diseases/therapy ; Autoimmunity ; B-Cell Activating Factor/immunology ; B-Cell Activation Factor Receptor/immunology ; B-Lymphocytes/immunology ; Homeostasis/immunology ; Humans ; Ligands ; Lymphocyte Activation/immunology
Chemical Substances	B-Cell Activating Factor ; B-Cell Activation Factor Receptor ; Ligands ; TNFRSF13C protein, human
Language	English
Publishing date	2006-11
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	7090-7
ISSN	1468-2060 ; 0003-4967
ISSN (online)	1468-2060
ISSN	0003-4967
DOI	10.1136/ard.2006.058412
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Article ; Online: pERKing up the BLIMP in plasma cell differentiation.

Allman, David M / Cancro, Michael P

Science signaling

2011 Volume 4, Issue 169, Page(s) pe21

Abstract: The intracellular pathways that induce the differentiation of naïve B cells into antibody-secreting plasma cells remain poorly defined. A new study now provides surprising evidence that the activation of extracellular signal-regulated kinase (ERK) is ... ...

Abstract	The intracellular pathways that induce the differentiation of naïve B cells into antibody-secreting plasma cells remain poorly defined. A new study now provides surprising evidence that the activation of extracellular signal-regulated kinase (ERK) is pivotal for inducing the transcriptional repressor B lymphocyte-induced maturation protein 1 (Blimp-1), which is required for plasma cell differentiation. Consequently, ERK-deficient B cells were unable to generate plasma cells effectively. This is an unexpected result, because previous work has shown that ERK signaling functions chiefly to induce cell division, whereas plasma cells are considered to be nondividing, terminally differentiated cells. This finding not only reveals an important signaling pathway that underlies antibody-mediated immunity but also raises important questions about the varying roles that ERK, and perhaps other kinases, may play in different biological contexts.
MeSH term(s)	Cell Differentiation/immunology ; Enzyme Activation/immunology ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Humans ; Models, Immunological ; Plasma Cells/immunology ; Positive Regulatory Domain I-Binding Factor 1 ; Repressor Proteins/metabolism ; Signal Transduction/immunology
Chemical Substances	Repressor Proteins ; PRDM1 protein, human (138415-26-6) ; Positive Regulatory Domain I-Binding Factor 1 (EC 2.1.1.-) ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24)
Language	English
Publishing date	2011-04-19
Publishing country	United States
Document type	Journal Article
ZDB-ID	2417226-1
ISSN	1937-9145 ; 1945-0877
ISSN (online)	1937-9145
ISSN	1945-0877
DOI	10.1126/scisignal.2001987
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Article: Acute Coronary Syndrome in Patients with SARS-CoV-2 Infection: Pathophysiology and Translational Perspectives.

Cancro, Francesco P / Bellino, Michele / Esposito, Luca / Romei, Stefano / Centore, Mario / D'Elia, Debora / Cristiano, Mario / Maglio, Angelantonio / Carrizzo, Albino / Rasile, Barbara / Alfano, Carmine / Vecchione, Carmine / Galasso, Gennaro

Translational medicine @ UniSa

2022 Volume 24, Issue 2, Page(s) 1–11

Abstract: Acute coronary syndromes (ACS) may complicate the clinical course of patients with Coronavirus Disease 2019 (COVID-19). It is still unclear whether this condition is a direct consequence of the primary disease. However, several mechanisms including ... ...

Abstract	Acute coronary syndromes (ACS) may complicate the clinical course of patients with Coronavirus Disease 2019 (COVID-19). It is still unclear whether this condition is a direct consequence of the primary disease. However, several mechanisms including direct cellular damage, endothelial dysfunction, in-situ thrombosis, systemic inflammatory response, and oxygen supply-demand imbalance have been described in patients with COVID-19. The onset of a prothrombotic state may also be facilitated by the endothelial dysfunction secondary to the systemic inflammatory response and to the direct viral cell damage. Moreover, dysfunctional endothelial cells may enhance vasospasm and platelet aggregation. The combination of these factors promotes atherosclerotic plaque instability, thrombosis and, consequently, type 1 myocardial infarction. Furthermore, severe hypoxia due to extensive pulmonary involvement, in association with other conditions described in COVID-19 such as sepsis, tachyarrhythmias, anemia, hypotension, and shock, may lead to mismatch between oxygen supply and demand, and cause type 2 myocardial infarction. A deeper understanding of the potential pathophysiological mechanisms underlying ACS in patients with COVID-19 could help the therapeutic management of these very high-risk patients.
Language	English
Publishing date	2022-08-29
Publishing country	Italy
Document type	Journal Article
ISSN	2239-9747
ISSN	2239-9747
DOI	10.37825/2239-9754.1034
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Article ; Online: Lipoprotein(a) levels and risk of adverse events after myocardial infarction in patients with and without diabetes.

Silverio, Angelo / Cancro, Francesco Paolo / Di Maio, Marco / Bellino, Michele / Esposito, Luca / Centore, Mario / Carrizzo, Albino / Di Pietro, Paola / Borrelli, Anna / De Luca, Giuseppe / Vecchione, Carmine / Galasso, Gennaro

Journal of thrombosis and thrombolysis

2022 Volume 54, Issue 3, Page(s) 382–392

Abstract: ... than patients without diabetes (p = 0.026). At a median follow-up of 1121 days, the primary outcome was reported ...

Abstract	Introduction: The aim of this study was to evaluate the association of lipoprotein(a) [Lp(a)] levels with long-term outcome in patients with recent history of myocardial infarction (MI), and to investigate if diabetes may influence this association. Methods: Consecutive MI patients who underwent urgent/emergent coronary angiography from February 2013 to June 2019 were prospectively collected. The primary outcome was the composite of MI recurrence and all-cause death. The propensity score weighting technique was used to account for covariates potentially influencing the relationship between Lp(a) levels and the study outcomes. Results: The study population consisted of 1018 post-MI patients (median age 63 years). Diabetes was reported in 280 patients (27.5%), who showed lower Lp(a) levels than patients without diabetes (p = 0.026). At a median follow-up of 1121 days, the primary outcome was reported in 182 patients (17.9%). At univariable Cox regression analysis, Lp(a) was associated with the risk of the primary outcome in the overall population and in non-diabetic patients, but not in diabetics. The adjusted Cox regression analysis confirmed the independent association between Lp(a) values and the primary outcome in non-diabetic patients, but not in diabetics.Lp(a) levels > 70 mg/dL were independently associated with the risk of the primary outcome in non-diabetic patients (adjusted HR: 2.839; 95% CI, 1.382-5.832), but not in diabetics. Conclusions: In this real-world post-MI population, increasing Lp(a) levels were significantly associated with the risk of recurrent MI and all-cause death, and very high Lp(a) serum concentration independently predicted long-term outcome in non-diabetic patients, but not in diabetics.
MeSH term(s)	Coronary Angiography ; Diabetes Mellitus ; Humans ; Lipoprotein(a)/blood ; Middle Aged ; Myocardial Infarction/etiology ; Risk Factors
Chemical Substances	LPA protein, human ; Lipoprotein(a)
Language	English
Publishing date	2022-09-20
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	1230645-9
ISSN	1573-742X ; 0929-5305
ISSN (online)	1573-742X
ISSN	0929-5305
DOI	10.1007/s11239-022-02701-w
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Article ; Online: Nucleoside-modified mRNA encoding HSV-2 glycoproteins C, D, and E prevents clinical and subclinical genital herpes.

Awasthi, Sita / Hook, Lauren M / Pardi, Norbert / Wang, Fushan / Myles, Arpita / Cancro, Michael P / Cohen, Gary H / Weissman, Drew / Friedman, Harvey M

Science immunology

2019 Volume 4, Issue 39

Abstract: The goals of a genital herpes vaccine are to prevent painful genital lesions and reduce or eliminate subclinical infection that risks transmission to partners and newborns. We evaluated a trivalent glycoprotein vaccine containing herpes simplex virus ... ...

Abstract	The goals of a genital herpes vaccine are to prevent painful genital lesions and reduce or eliminate subclinical infection that risks transmission to partners and newborns. We evaluated a trivalent glycoprotein vaccine containing herpes simplex virus type 2 (HSV-2) entry molecule glycoprotein D (gD2) and two immune evasion molecules: glycoprotein C (gC2), which binds complement C3b, and glycoprotein E (gE2), which blocks immunoglobulin G (IgG) Fc activities. The trivalent vaccine was administered as baculovirus proteins with CpG and alum, or the identical amino acids were expressed using nucleoside-modified mRNA in lipid nanoparticles (LNPs). Both formulations completely prevented genital lesions in mice and guinea pigs. Differences emerged when evaluating subclinical infection. The trivalent protein vaccine prevented dorsal root ganglia infection, and day 2 and 4 vaginal cultures were negative in 23 of 30 (73%) mice compared with 63 of 64 (98%) in the mRNA group (
MeSH term(s)	Animals ; Guinea Pigs ; Herpes Genitalis/immunology ; Nucleosides/immunology ; RNA, Messenger/biosynthesis ; RNA, Messenger/immunology ; Viral Envelope Proteins/biosynthesis ; Viral Envelope Proteins/immunology
Chemical Substances	Nucleosides ; RNA, Messenger ; Viral Envelope Proteins ; glycoprotein C, herpes simplex virus type 2 ; glycoprotein D-herpes simplex virus type 2
Language	English
Publishing date	2019-09-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	2470-9468
ISSN (online)	2470-9468
DOI	10.1126/sciimmunol.aaw7083
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Article ; Online: The E3 ubiquitin ligase Itch restricts antigen-driven B cell responses.

Moser, Emily K / Roof, Jennifer / Dybas, Joseph M / Spruce, Lynn A / Seeholzer, Steven H / Cancro, Michael P / Oliver, Paula M

The Journal of experimental medicine

2019 Volume 216, Issue 9, Page(s) 2170–2183

Abstract: The E3 ubiquitin ligase Itch regulates antibody levels and prevents autoimmune disease in humans and mice, yet how Itch regulates B cell fate or function is unknown. We now show that Itch directly limits B cell activity. While Itch-deficient mice ... ...

Abstract	The E3 ubiquitin ligase Itch regulates antibody levels and prevents autoimmune disease in humans and mice, yet how Itch regulates B cell fate or function is unknown. We now show that Itch directly limits B cell activity. While Itch-deficient mice displayed normal numbers of preimmune B cell populations, they showed elevated numbers of antigen-experienced B cells. Mixed bone marrow chimeras revealed that Itch acts within B cells to limit naive and, to a greater extent, germinal center (GC) B cell numbers. B cells lacking Itch exhibited increased proliferation, glycolytic capacity, and mTORC1 activation. Moreover, stimulation of these cells in vivo by WT T cells resulted in elevated numbers of GC B cells, PCs, and serum IgG. These results support a novel role for Itch in limiting B cell metabolism and proliferation to suppress antigen-driven B cell responses.
MeSH term(s)	Animals ; Antibodies/blood ; Antibody Formation/immunology ; Antigens/metabolism ; B-Lymphocytes/immunology ; Cell Cycle ; Cell Proliferation ; Germinal Center/immunology ; Immunization ; Lymphocyte Activation/immunology ; Lymphocyte Count ; Mechanistic Target of Rapamycin Complex 1/metabolism ; Mice, Knockout ; Proteomics ; Ubiquitin-Protein Ligases/metabolism
Chemical Substances	Antibodies ; Antigens ; Itch protein, mouse (EC 2.3.2.26) ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1)
Language	English
Publishing date	2019-07-16
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	218343-2
ISSN	1540-9538 ; 0022-1007
ISSN (online)	1540-9538
ISSN	0022-1007
DOI	10.1084/jem.20181953
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Article ; Online: TACI expression and plasma cell differentiation are impaired in the absence of functional IκBNS.

Khoenkhoen, Sharesta / Erikson, Elina / Ádori, Monika / Stark, Julian M / Scholz, Jean L / Cancro, Michael P / Pedersen, Gabriel K / Karlsson Hedestam, Gunilla B

Immunology and cell biology

2019 Volume 97, Issue 5, Page(s) 485–497

Abstract: Impaired classical NF-κB pathway signaling causes reduced antibody responses to T-independent (TI) antigens. We investigated the potential reasons for defective TI responses in mice lacking the atypical inhibitory kappa B (IκB) protein of the NF-κB ... ...

Abstract	Impaired classical NF-κB pathway signaling causes reduced antibody responses to T-independent (TI) antigens. We investigated the potential reasons for defective TI responses in mice lacking the atypical inhibitory kappa B (IκB) protein of the NF-κB pathway, IκBNS. Analyses of the plasma cell compartment in vitro and in vivo after challenge with lipopolysaccharide (LPS) showed significant decreases in the frequencies of plasma cells in the absence of IκBNS. In vitro activation of B cells via the B cell receptor or via Toll-like receptor 4 revealed that early activation events were unaffected in IκBNS-deficient B cells, while proliferation was reduced compared to in similarly stimulated wildtype (wt) B cells. IκBNS-deficient B cells also displayed impaired upregulation of the transmembrane activator and calcium modulator cyclophilin ligand interactor (TACI), which is essential for TI responses, and decreased sensitivity to TACI ligands upon stimulation. Furthermore, IκBNS-deficient B cells, in contrast to wt B cells, displayed altered expression of IRF4, Blimp-1 and Pax5 upon LPS-induced differentiation, indicating impaired transcriptional regulation of plasma cell generation.
MeSH term(s)	Animals ; Cell Differentiation/genetics ; Cell Differentiation/immunology ; Gene Expression Regulation/immunology ; I-kappa B Proteins/deficiency ; I-kappa B Proteins/immunology ; Mice ; Mice, Knockout ; Plasma Cells/cytology ; Plasma Cells/immunology ; Toll-Like Receptor 4/genetics ; Toll-Like Receptor 4/immunology ; Transmembrane Activator and CAML Interactor Protein/genetics ; Transmembrane Activator and CAML Interactor Protein/immunology
Chemical Substances	I-kappa B Proteins ; Nfkbid protein, mouse ; Tlr4 protein, mouse ; Tnfrsf13b protein, mouse ; Toll-Like Receptor 4 ; Transmembrane Activator and CAML Interactor Protein
Language	English
Publishing date	2019-01-30
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	284057-1
ISSN	1440-1711 ; 0818-9641
ISSN (online)	1440-1711
ISSN	0818-9641
DOI	10.1111/imcb.12228
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Book: BLyS ligands and receptors

Cancro, M. P

(Contemporary immunology)

2010

Author's details	Michael P. Cancro, editor
Series title	Contemporary immunology
MeSH term(s)	B-Lymphocytes/cytology ; Ligands ; Receptors, Cell Surface/immunology ; Cell Differentiation/immunology
Language	English
Size	xiii, 289 p. :, ill. ;, 25 cm.
Publisher	Humana Press
Publishing place	New York
Document type	Book
ISBN	9781603270120 ; 1603270124 ; 9781603270137 ; 1603270132
Database	Catalogue of the US National Library of Medicine (NLM)

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