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Article ; Online: The spleen: "epicenter" in malaria infection and immunity.

Ghosh, Debopam / Stumhofer, Jason S

2021 Volume 110, Issue 4, Page(s) 753–769

Abstract: The spleen is a complex secondary lymphoid organ that plays a crucial role in controlling blood-stage infection with Plasmodium parasites. It is tasked with sensing and removing parasitized RBCs, erythropoiesis, the activation and differentiation of ... ...

Abstract	The spleen is a complex secondary lymphoid organ that plays a crucial role in controlling blood-stage infection with Plasmodium parasites. It is tasked with sensing and removing parasitized RBCs, erythropoiesis, the activation and differentiation of adaptive immune cells, and the development of protective immunity, all in the face of an intense inflammatory environment. This paper describes how these processes are regulated following infection and recognizes the gaps in our current knowledge, highlighting recent insights from human infections and mouse models.
MeSH term(s)	Animals ; Erythrocytes/parasitology ; Hematopoiesis ; Humans ; Immunity ; Malaria/immunology ; Malaria/parasitology ; Malaria/prevention & control ; Plasmodium/physiology ; Spleen/immunology ; Spleen/parasitology ; Spleen/pathology
Language	English
Publishing date	2021-01-19
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	605722-6
ISSN	1938-3673 ; 0741-5400
ISSN (online)	1938-3673
ISSN	0741-5400
DOI	10.1002/JLB.4RI1020-713R
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Article ; Online: New insights into B cells as antigen presenting cells.

Ghosh, Debopam / Jiang, Wei / Mukhopadhyay, Dhriti / Mellins, Elizabeth D

Current opinion in immunology

2021 Volume 70, Page(s) 129–137

Abstract: In addition to their role as antibody producing cells, B cells make a critical contribution to adaptive immune responses by functioning as professional antigen-presenting cells (APC). Distinctive features of B cells as APC include the expression of the B ...

Abstract	In addition to their role as antibody producing cells, B cells make a critical contribution to adaptive immune responses by functioning as professional antigen-presenting cells (APC). Distinctive features of B cells as APC include the expression of the B cell receptor (BCR) for antigen and regulated expression of HLA-DO. Here, we discuss recent progress in investigation of B cells as APC. We start with an update on the canonical MHC class II antigen presentation pathway in B cells and alternative pathways, including generation of extracellular vesicles. Turning to APC function, we highlight the roles of B cells as thymic APC, as APC for T follicular helper (T
MeSH term(s)	Animals ; Antigen-Presenting Cells/immunology ; B-Lymphocytes/immunology ; Humans
Language	English
Publishing date	2021-07-06
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1035767-1
ISSN	1879-0372 ; 0952-7915
ISSN (online)	1879-0372
ISSN	0952-7915
DOI	10.1016/j.coi.2021.06.003
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Article ; Online: Harnessing IgG Fc glycosylation for clinical benefit.

Archer, Eva J / Gonzalez, Joseph C / Ghosh, Debopam / Mellins, Elizabeth D / Wang, Taia T

Current opinion in immunology

2022 Volume 77, Page(s) 102231

Abstract: The effector activity of IgG antibodies is regulated at several levels, including IgG subclass, modifications of the Fc glycan, and the distribution of Type I and II Fcγ receptors (FcγR) on effector cells. Here, we explore how Fc glycosylation, ... ...

Abstract	The effector activity of IgG antibodies is regulated at several levels, including IgG subclass, modifications of the Fc glycan, and the distribution of Type I and II Fcγ receptors (FcγR) on effector cells. Here, we explore how Fc glycosylation, particularly sialylation and fucosylation, tunes cellular responses to immune complexes. We review the current understanding of the pathways and mechanisms underlying this biology, address FcγR in antigen presentation, and discuss aspects of the clinical understanding of Fc glycans in therapies and disease.
MeSH term(s)	Antigen-Antibody Complex/metabolism ; Glycosylation ; Humans ; Immunoglobulin Fc Fragments ; Immunoglobulin G/metabolism ; Polysaccharides ; Receptors, IgG
Chemical Substances	Antigen-Antibody Complex ; Immunoglobulin Fc Fragments ; Immunoglobulin G ; Polysaccharides ; Receptors, IgG
Language	English
Publishing date	2022-07-04
Publishing country	England
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1035767-1
ISSN	1879-0372 ; 0952-7915
ISSN (online)	1879-0372
ISSN	0952-7915
DOI	10.1016/j.coi.2022.102231
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Article: Do you see what I see: Recognition of protozoan parasites by Toll-like receptors.

Ghosh, Debopam / Stumhofer, Jason S

Current immunology reviews

2014 Volume 9, Issue 3, Page(s) 129–140

Abstract: Toll-like receptors (TLRs) are important for recognizing a variety of pathogens, including protozoan parasites, and initiating innate immune responses against them. TLRs are localized on the cell surface as well as in the endosome, and are implicated in ... ...

Abstract	Toll-like receptors (TLRs) are important for recognizing a variety of pathogens, including protozoan parasites, and initiating innate immune responses against them. TLRs are localized on the cell surface as well as in the endosome, and are implicated in innate sensing of these parasites. In this review, we will discuss recent findings on the identification of parasite-derived pathogen associated molecular patterns and the TLRs that bind them. The role of these TLRs in initiating the immune response against protozoan parasitic infections
Language	English
Publishing date	2014-05-14
Publishing country	United Arab Emirates
Document type	Journal Article
ZDB-ID	2274820-9
ISSN	1875-631X ; 1573-3955
ISSN (online)	1875-631X
ISSN	1573-3955
DOI	10.2174/1573395509666131203225929
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Article: Intrinsic p53 Activation Restricts Gammaherpesvirus-Driven Germinal Center B Cell Expansion during Latency Establishment.

Owens, Shana M / Sifford, Jeffrey M / Li, Gang / Murdock, Steven J / Salinas, Eduardo / Manzano, Mark / Ghosh, Debopam / Stumhofer, Jason S / Forrest, J Craig

bioRxiv : the preprint server for biology

2023

Abstract: Gammaherpesviruses (GHV) are DNA tumor viruses that establish lifelong latent infections in lymphocytes. For viruses such as Epstein-Barr virus (EBV) and murine gammaherpesvirus 68 (MHV68), this is accomplished through a viral gene-expression program ... ...

Abstract	Gammaherpesviruses (GHV) are DNA tumor viruses that establish lifelong latent infections in lymphocytes. For viruses such as Epstein-Barr virus (EBV) and murine gammaherpesvirus 68 (MHV68), this is accomplished through a viral gene-expression program that promotes cellular proliferation and differentiation, especially of germinal center (GC) B cells. Intrinsic host mechanisms that control virus-driven cellular expansion are incompletely defined. Using a small-animal model of GHV pathogenesis, we demonstrate Importance: Gammaherpesviruses cause lifelong infections of their hosts, commonly referred to as latency, that can lead to cancer. Latency establishment benefits from the functions of viral proteins that augment and amplify B cell activation, proliferation, and differentiation signals. In uninfected cells, off-schedule cellular differentiation would typically trigger anti-proliferative responses by effector proteins known as tumor suppressors. However, tumor suppressor responses to gammaherpesvirus manipulation of cellular processes remain understudied, especially those that occur during latency establishment in a living organism. Here we identify p53, a tumor suppressor commonly mutated in cancer, as a host factor that limits virus-driven B cell proliferation and differentiation, and thus, viral colonization of a host. We demonstrate that p53 activation occurs in response to viral latency proteins that induce B cell activation. This work informs a gap in our understanding of intrinsic cellular defense mechanisms that restrict lifelong GHV infection.
Language	English
Publishing date	2023-11-01
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.10.31.563188
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Article ; Online: IL-17 Promotes Differentiation of Splenic LSK

Ghosh, Debopam / Brown, Susie L / Stumhofer, Jason S

Journal of immunology (Baltimore, Md. : 1950)

2017 Volume 199, Issue 5, Page(s) 1783–1795

Abstract: ... ...

Abstract	Lineage
MeSH term(s)	Animals ; Antibodies, Protozoan/metabolism ; Antibody-Producing Cells/parasitology ; Antibody-Producing Cells/physiology ; B-Lymphocytes/parasitology ; B-Lymphocytes/physiology ; Cell Differentiation ; Cells, Cultured ; Chemokine CXCL12/metabolism ; Female ; Humans ; Immunologic Memory ; Interleukin-17/metabolism ; Lymphoid Progenitor Cells/parasitology ; Lymphoid Progenitor Cells/physiology ; Malaria/immunology ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Knockout ; Plasmodium yoelii/immunology ; Proto-Oncogene Proteins pp60(c-src)/metabolism ; Receptors, Interleukin-17/genetics ; Spleen/immunology
Chemical Substances	Antibodies, Protozoan ; Chemokine CXCL12 ; Il17r protein, mouse ; Interleukin-17 ; Receptors, Interleukin-17 ; Matk protein, mouse (EC 2.7.1.-) ; Proto-Oncogene Proteins pp60(c-src) (EC 2.7.10.2)
Language	English
Publishing date	2017-07-21
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.1601972
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Article ; Online: Pulse-Chase Analysis for Studies of MHC Class II Biosynthesis, Maturation, and Peptide Loading.

Hou, Tieying / Rinderknecht, Cornelia / Ghosh, Debopam / Hadjinicolaou, Andreas V / Busch, Robert / Mellins, Elizabeth D

Methods in molecular biology (Clifton, N.J.)

2019 Volume 1988, Page(s) 315–341

Abstract: Pulse-chase analysis is a commonly used technique for studying the synthesis, processing, and transport of proteins. Cultured cells expressing proteins of interest are allowed to take up radioactively labeled amino acids for a brief interval ("pulse"), ... ...

Abstract	Pulse-chase analysis is a commonly used technique for studying the synthesis, processing, and transport of proteins. Cultured cells expressing proteins of interest are allowed to take up radioactively labeled amino acids for a brief interval ("pulse"), during which all newly synthesized proteins incorporate the label. The cells are then returned to nonradioactive culture medium for various times ("chase"), during which proteins may undergo conformational changes, trafficking, or degradation. Proteins of interest are isolated (usually by immunoprecipitation) and resolved by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE), and the fate of radiolabeled molecules is examined by autoradiography. This chapter describes a pulse-chase protocol suitable for studies of major histocompatibility complex (MHC) class II biosynthesis and maturation. We discuss how results are affected by the recognition by certain anti-class II antibodies of distinct class II conformations associated with particular biosynthetic states. Our protocol can be adapted to follow the fate of many other endogenously synthesized proteins, including viral or transfected gene products, in cultured cells.
MeSH term(s)	Animals ; Antibodies/metabolism ; Cell Line ; Detergents ; Electrophoresis, Polyacrylamide Gel ; Histocompatibility Antigens Class II/biosynthesis ; Histocompatibility Antigens Class II/metabolism ; Humans ; Mice ; Molecular Biology/methods ; Peptides/metabolism
Chemical Substances	Antibodies ; Detergents ; Histocompatibility Antigens Class II ; Peptides
Language	English
Publishing date	2019-05-30
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-4939-9450-2_23
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Article: Signaling Circuits and Regulation of Immune Suppression by Ovarian Tumor-Associated Macrophages.

Cannon, Martin J / Ghosh, Debopam / Gujja, Swetha

Vaccines

2015 Volume 3, Issue 2, Page(s) 448–466

Abstract: The barriers presented by immune suppression in the ovarian tumor microenvironment present one of the biggest challenges to development of successful tumor vaccine strategies for prevention of disease recurrence and progression following primary surgery ... ...

Abstract	The barriers presented by immune suppression in the ovarian tumor microenvironment present one of the biggest challenges to development of successful tumor vaccine strategies for prevention of disease recurrence and progression following primary surgery and chemotherapy. New insights gained over the last decade have revealed multiple mechanisms of immune regulation, with ovarian tumor-associated macrophages/DC likely to fulfill a central role in creating a highly immunosuppressive milieu that supports disease progression and blocks anti-tumor immunity. This review provides an appraisal of some of the key signaling pathways that may contribute to immune suppression in ovarian cancer, with a particular focus on the potential involvement of the c-KIT/PI3K/AKT, wnt/β-catenin, IL-6/STAT3 and AhR signaling pathways in regulation of indoleamine 2,3-dioxygenase expression in tumor-associated macrophages. Knowledge of intercellular and intracellular circuits that shape immune suppression may afford insights for development of adjuvant treatments that alleviate immunosuppression in the tumor microenvironment and enhance the clinical efficacy of ovarian tumor vaccines.
Language	English
Publishing date	2015-05-29
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2703319-3
ISSN	2076-393X
ISSN	2076-393X
DOI	10.3390/vaccines3020448
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Article ; Online: The Costimulatory Molecule ICOS Regulates Host Th1 and Follicular Th Cell Differentiation in Response to Plasmodium chabaudi chabaudi AS Infection.

Wikenheiser, Daniel J / Ghosh, Debopam / Kennedy, Brian / Stumhofer, Jason S

Journal of immunology (Baltimore, Md. : 1950)

2016 Volume 196, Issue 2, Page(s) 778–791

Abstract: Blood-stage Plasmodium chabaudi chabaudi AS infection requires cell- and Ab-mediated immunity to control acute and persistent infection, respectively. ICOS regulates CD4(+) T cell activation and promotes the induction of follicular Th (TFH) cells, CD4(+) ...

Abstract	Blood-stage Plasmodium chabaudi chabaudi AS infection requires cell- and Ab-mediated immunity to control acute and persistent infection, respectively. ICOS regulates CD4(+) T cell activation and promotes the induction of follicular Th (TFH) cells, CD4(+) T cells that support B cell affinity maturation within germinal centers (GCs), resulting in the production of high-affinity Abs. In this article, we demonstrate that, in response to P. c. chabaudi AS infection, the absence of ICOS resulted in an enhanced Th1 immune response that reduced peak parasitemia. Despite the absence of ICOS, CD4(+) T cells were capable of expressing PD-1, B cell lymphoma 6, and CXCR5 during early infection, indicating TFH development was not impaired. However, by day 21 postinfection, Icos(-/-) mice accumulated fewer splenic TFHs compared with Icos(+/+) mice, leading to substantially fewer GC B cells and a decrease in affinity, but not production, of parasite-specific isotype-switched Abs. Moreover, treatment of mice with anti-ICOS ligand Abs to modulate ICOS-ICOS ligand signaling revealed a requirement for ICOS in TFH differentiation only after day 6 postinfection. Ultimately, the quality and quantity of isotype-switched Abs produced in Icos(-/-) mice declined over time, resulting in impaired control of persistent parasitemia. Collectively, these data suggest ICOS is not required for TFH induction during P. c. chabaudi AS infection or production of isotype-switched Abs, but it is necessary for maintenance of a sustained high-affinity, protective Ab response.
MeSH term(s)	Animals ; Cell Differentiation/immunology ; Disease Models, Animal ; Enzyme-Linked Immunosorbent Assay ; Flow Cytometry ; Fluorescent Antibody Technique ; Germinal Center/cytology ; Germinal Center/immunology ; Inducible T-Cell Co-Stimulator Protein/immunology ; Lymphocyte Activation/immunology ; Malaria/immunology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Plasmodium chabaudi ; T-Lymphocyte Subsets/immunology ; T-Lymphocytes, Helper-Inducer/immunology ; Th1 Cells/immunology
Chemical Substances	Icos protein, mouse ; Inducible T-Cell Co-Stimulator Protein
Language	English
Publishing date	2016-01-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
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.1403206
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Article ; Online: Regulation of the BCR signalosome by the class II peptide editor, H2-M, affects the development and repertoire of innate-like B cells.

Ghosh, Debopam / Pham, Tho D / Nanaware, Padma P / Sengupta, Deepanwita / Adler, Lital N / Li, Caiyun G / He, Xiao / O'Mara, Mary E / Kantor, Aaron B / Nguyen, Khoa D / Yang, Yang / Eisenlohr, Laurence C / Jensen, Peter E / Herzenberg, Leonore A / Stern, Lawrence J / Boyd, Scott D / Ghosn, Eliver E B / Mellins, Elizabeth D

Cell reports

2022 Volume 38, Issue 4, Page(s) 110200

Abstract: The non-classical Major Histocompatibility Complex class II (MHCII) protein, H2-M, edits peptides bound to conventional MHCII in favor of stable peptide/MHCII (p/MHCII) complexes. Here, we show that H2-M deficiency affects B-1 cell survival, reduces cell ...

Abstract	The non-classical Major Histocompatibility Complex class II (MHCII) protein, H2-M, edits peptides bound to conventional MHCII in favor of stable peptide/MHCII (p/MHCII) complexes. Here, we show that H2-M deficiency affects B-1 cell survival, reduces cell renewal capacity, and alters immunoglobulin repertoire, allowing for the selection of cells specific for highly abundant epitopes, but not low-frequency epitopes. H2-M-deficient B-1 cells have shorter CDR3 length, higher content of positively charged amino acids, shorter junctional regions, less mutation frequency, and a skewed clonal distribution. Mechanistically, H2-M loss reduces plasma membrane p/MHCII association with B cell receptors (BCR) on B-1 cells and diminishes integrated BCR signal strength, a key determinant of B-1 cell selection, maturation, and maintenance. Thus, H2-M:MHCII interaction serves as a cell-intrinsic regulator of BCR signaling and influences the selection of the B-1 cell clonal repertoire.
MeSH term(s)	Animals ; B-Lymphocytes/immunology ; Histocompatibility Antigens Class II/immunology ; Lymphocyte Activation/immunology ; Mice ; Receptors, Antigen, B-Cell/immunology
Chemical Substances	H2-M antigens ; Histocompatibility Antigens Class II ; Receptors, Antigen, B-Cell
Language	English
Publishing date	2022-01-26
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2021.110200
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