scholarly journals B Cells Control Mucosal-Associated Invariant T Cell Responses to Salmonella enterica Serovar Typhi Infection Through the CD85j HLA-G Receptor

2021 ◽  
Vol 12 ◽  
Author(s):  
Rosângela Salerno-Gonçalves ◽  
Tasmia Rezwan ◽  
David Luo ◽  
Hervé Tettelin ◽  
Marcelo B. Sztein
Keyword(s):  
B Cells ◽  
Salmonella Enterica ◽  
Kinetic Studies ◽  
Salmonella Enterica Serovar Typhi ◽  
Mait Cells ◽  
Cell Responses ◽  
Ifn Γ ◽  
And Function ◽  
First Time ◽  
Mait Cell

Mucosal-associated invariant T (MAIT) cells are an innate-like population of T cells that display a TCR Vα7.2+ CD161+ phenotype and are restricted by the nonclassical MHC-related molecule 1 (MR1). Although B cells control MAIT cell development and function, little is known about the mechanisms underlying their interaction(s). Here, we report, for the first time, that during Salmonella enterica serovar Typhi (S. Typhi) infection, HLA-G expression on B cells downregulates IFN-γ production by MAIT cells. In contrast, blocking HLA-G expression on S. Typhi-infected B cells increases IFN-γ production by MAIT cells. After interacting with MAIT cells, kinetic studies show that B cells upregulate HLA-G expression and downregulate the inhibitory HLA-G receptor CD85j on MAIT cells resulting in their loss. These results provide a new role for HLA-G as a negative feedback loop by which B cells control MAIT cell responses to antigens.

scholarly journals TLR7 modulating B-cell immune responses in the spleen of C57BL/6 mice infected with Schistosoma japonicum

2021 ◽  
Vol 15 (11) ◽  
pp. e0009943
Author(s):  
Haixia Wei ◽  
Hongyan Xie ◽  
Jiale Qu ◽  
Anqi Xie ◽  
Shihao Xie ◽  
...  
Keyword(s):  
B Cells ◽  
B Cell ◽  
Gene Knockout ◽  
Innate Immune ◽  
Wild Type ◽  
Cell Responses ◽  
Splenic Cells ◽  
And Function ◽  
Egg Antigen

B cells played an important role in Schistosoma infection-induced diseases. TLR7 is an intracellular member of the innate immune receptor. The role of TLR7 on B cells mediated immune response is still unclear. Here, C57BL/6 mice were percutaneously infected by S. japonicum for 5–6 weeks. The percentages and numbers of B cells increased in the infected mice (p < 0.05), and many activation and function associated molecules were also changed on B cells. More splenic cells of the infected mice expressed TLR7, and B cells were served as the main cell population. Moreover, a lower level of soluble egg antigen (SEA) specific antibody and less activation associated molecules were found on the surface of splenic B cells from S. japonicum infected TLR7 gene knockout (TLR7 KO) mice compared to infected wild type (WT) mice (p < 0.05). Additionally, SEA showed a little higher ability in inducing the activation of B cells from naive WT mice than TLR7 KO mice (p < 0.05). Finally, the effects of TLR7 on B cells are dependent on the activation of NF-κB p65. Altogether, TLR7 was found modulating the splenic B cell responses in S. japonicum infected C57BL/6 mice.

CD8 T cells induce T-bet–dependent migration toward CXCR3 ligands by differentiated B cells produced during responses to alum-protein vaccines

Blood ◽  
2012 ◽  
Vol 120 (23) ◽  
pp. 4552-4559 ◽  
Author(s):  
Karine Serre ◽  
Adam F. Cunningham ◽  
Ruth E. Coughlan ◽  
Andreia C. Lino ◽  
Antal Rot ◽  
...  
Keyword(s):  
T Cells ◽  
B Cells ◽  
Cd8 T Cells ◽  
Cd4 T Cell ◽  
T Helper ◽  
T Helper 2 ◽  
Cell Responses ◽  
Cxcr3 Expression ◽  
Ifn Γ ◽  
Draining Lymph Nodes

Abstract Antibody-forming cells (AFCs) expressing the chemokine receptor CXCR3 are recruited to sites of inflammation where they help clear pathogens but may participate in autoimmune diseases. Here we identify a mechanism that induces CXCR3 expression by AFC and germinal center (GC) B cells. This happens when CD8 T cells are recruited into CD4 T cell–dependent B-cell responses. Ovalbumin-specific CD4 T cells (OTII) were transferred alone or with ovalbumin-specific CD8 T cells (OTI) and the response to subcutaneous alum-precipitated ovalbumin was followed in the draining lymph nodes. OTII cells alone induce T helper 2-associated class switching to IgG1, but few AFC or GC B cells express CXCR3. By contrast, OTI-derived IFN-γ induces most responding GC B cells and AFCs to express high levels of CXCR3, and diverse switching to IgG2a, IgG2b, with some IgG1. Up-regulation of CXCR3 by GC B cells and AFCs and their migration toward its ligand CXCL10 are shown to depend on B cells' intrinsic T-bet, a transcription factor downstream of the IFN-γR signaling. This model clarifies how precursors of long-lived AFCs and memory B cells acquire CXCR3 that causes their migration to inflammatory foci.

scholarly journals Legionella protection and vaccination mediated by Mucosal Associated Invariant T (MAIT) cells

2017 ◽  
Author(s):  
Huimeng Wang ◽  
Criselle D’Souza ◽  
Xin Yi Lim ◽  
Lyudmila Kostenko ◽  
Troi J Pediongco ◽  
...  
Keyword(s):  
Cell Activation ◽  
Cell Protection ◽  
Gm Csf ◽  
Mait Cells ◽  
Cell Immunity ◽  
Tnf Α ◽  
Ifn Γ ◽  
Clinically Significant ◽  
Riboflavin Synthesis ◽  
Mait Cell

AbstractMucosal associated invariant T (MAIT) cells recognize conserved microbial metabolites from riboflavin synthesis. Striking evolutionary conservation and pulmonary abundance implicate them in antibacterial host defense, yet their roles in protection against clinically significant pathogens are unknown. Murine Legionella infection induced MR1-dependent MAIT cell activation and rapid pulmonary accumulation of MAIT cells associated with immune protection detectable in fully immunocompetent host animals. MAIT cell protection was more evident in mice lacking CD4+ cells, whilst profoundly immunodeficient RAG2−/−γC−/− mice were substantially rescued from uniformly lethal Legionella infection by adoptively-transferred MAIT cells. This protection was dependent on MR1, IFN-γ and GM-CSF, but not IL-17, TNF-α or perforin. Protection was enhanced and observed earlier post-infection in mice that were Ag-primed to boost MAIT cells before infection. Our findings define a significant role for MAIT cells in protection against a major human pathogen and indicate a potential role for vaccination to enhance MAIT cell immunity.

scholarly journals MicroRNA-155 Regulates MAIT1 and MAIT17 Cell Differentiation

2021 ◽  
Vol 9 ◽  
Author(s):  
Tingting Liu ◽  
Jie Wang ◽  
Kalpana Subedi ◽  
Qijun Yi ◽  
Li Zhou ◽  
...  
Keyword(s):  
Immune Cell ◽  
Cell Lineage ◽  
Cell Development ◽  
Loss Of Function ◽  
Mait Cells ◽  
Cellular Processes ◽  
Individual Mirnas ◽  
Maturation Stages ◽  
And Function ◽  
Mait Cell

Mucosal-associated invariant T (MAIT) cells are innate-like T cells that develop in the thymus through three maturation stages to acquire effector function and differentiate into MAIT1 (T-bet+) and MAIT17 (RORγt+) subsets. Upon activation, MAIT cells release IFN-γ and IL-17, which modulate a broad spectrum of diseases. Recent studies indicate defective MAIT cell development in microRNA deficient mice, however, few individual miRNAs have been identified to regulate MAIT cells. MicroRNA-155 (miR-155) is a key regulator of numerous cellular processes that affect some immune cell development, but its role in MAIT cell development remains unclear. To address whether miR-155 is required for MAIT cell development, we performed gain-of-function and loss-of-function studies. We first generated a CD4Cre.miR-155 knock-in mouse model, in which miR-155 is over-expressed in the T cell lineage. We found that overexpression of miR-155 significantly reduced numbers and frequencies of MAIT cells in all immune organs and lungs and blocked thymic MAIT cell maturation through downregulating PLZF expression. Strikingly, upregulated miR-155 promoted MAIT1 differentiation and blocked MAIT17 differentiation, and timely inducible expression of miR-155 functionally inhibited peripheral MAIT cells secreting IL-17. miR-155 overexpression also increased CD4–CD8+ subset and decreased CD4–CD8– subset of MAIT cells. We further analyzed MAIT cells in conventional miR-155 knockout mice and found that lack of miR-155 also promoted MAIT1 differentiation and blocked MAIT17 differentiation but without alteration of their overall frequency, maturation and function. Overall, our results indicate that adequate miR-155 expression is required for normal MAIT1 and MAIT17 cell development and function.

scholarly journals Sustained IFN-I stimulation impairs MAIT cell responses to bacteria by inducing IL-10 during chronic HIV-1 infection

2020 ◽  
Vol 6 (8) ◽  
pp. eaaz0374 ◽  
Author(s):  
X. Tang ◽  
S. Zhang ◽  
Q. Peng ◽  
L. Ling ◽  
H. Shi ◽  
...  
Keyword(s):  
Cell Activation ◽  
Surface Protein ◽  
Interleukin 10 ◽  
Mait Cells ◽  
Cell Dysfunction ◽  
Cell Responses ◽  
High Level ◽  
Hiv 1 ◽  
Mait Cell

Mucosal-associated invariant T (MAIT) cells in HIV-1–infected individuals are functionally impaired by poorly understood mechanisms. Single-cell transcriptional and surface protein analyses revealed that peripheral MAIT cells from HIV-1–infected subjects were highly activated with the up-regulation of interferon (IFN)–stimulated genes as compared to healthy individuals. Sustained IFN-α treatment suppressed MAIT cell responses to Escherichia coli by triggering high-level interleukin-10 (IL-10) production by monocytes, which subsequently inhibited the secretion of IL-12, a crucial costimulatory cytokine for MAIT cell activation. Blocking IFN-α or IL-10 receptors prevented MAIT cell dysfunction induced by HIV-1 exposure in vitro. Moreover, blocking the IL-10 receptor significantly improved anti–Mycobacterium tuberculosis responses of MAIT cells from HIV-1–infected patients. Our findings demonstrate the central role of the IFN-I/IL-10 axis in MAIT cell dysfunction during HIV-1 infection, which has implications for the development of anti–IFN-I/IL-10 strategies against bacterial coinfections in HIV-1–infected patients.

scholarly journals Characterization and Development of T-Cell Immune Responses in B-Cell-Deficient (Igh-6−/−) Mice with Salmonella enterica Serovar TyphimuriumInfection

2003 ◽  
Vol 71 (12) ◽  
pp. 6808-6819 ◽  
Author(s):  
Sanja Ugrinovic ◽  
Nathalie Ménager ◽  
Natalie Goh ◽  
Pietro Mastroeni
Keyword(s):  
T Cells ◽  
T Cell ◽  
B Cells ◽  
B Cell ◽  
Salmonella Enterica ◽  
Early Stage ◽  
T Cell Responses ◽  
Costimulatory Molecules ◽  
Cell Responses ◽  
Serovar Typhimurium

ABSTRACT Infection of mice with Salmonella enterica serovar Typhimurium induces strong Th1 T-cell responses that are central to the control of the infection. In the present study, we examined the role of B cells in the development of Th1 T-cell responses to Salmonella by using gene-targeted B-cell-deficient mice (Igh-6−/− mice). The development of Th1 T-cell responses in Igh-6−/− mice was impaired in the early stage of a primary infection. This impairment persisted throughout the course of the disease. The ability of T cells to produce the Th1 cytokine gamma interferon and the frequency at which they did so were lower in Igh-6−/− mice than in control mice. We also observed a transient switch toward Th2 cytokine production in Igh-6−/− mice. Thus, B cells are important for the induction of protective Th1 T-cell responses in the early phase of a Salmonella infection. Activated B cells express high levels of major histocompatibility complex and costimulatory molecules and are nearly as effective as dendritic cells in their antigen-presenting cell (APC) activity. However, their importance as APCs in infection and their role in initiating and/or maintaining T-cell responses are unknown. Here, we show that B cells upregulate costimulatory molecules upon in vitro stimulation with S. enterica serovar Typhimurium and that they can present Salmonella antigens to Salmonella-specific CD4+ T cells. Our results show that B cells are important for the development of T-cell responses in the early stage of a Salmonella infection and that this property may be due to their ability to present antigens to T cells.

scholarly journals Salmonella enterica Serovar Typhi Possesses a Unique Repertoire of Fimbrial Gene Sequences

2001 ◽  
Vol 69 (5) ◽  
pp. 2894-2901 ◽  
Author(s):  
Stacy M. Townsend ◽  
Naomi E. Kramer ◽  
Robert Edwards ◽  
Stephen Baker ◽  
Nancy Hamlin ◽  
...  
Keyword(s):  
Host Range ◽  
Salmonella Enterica ◽  
Host Adaptation ◽  
Unique Combination ◽  
Gene Sequences ◽  
Simple Correlation ◽  
Salmonella Enterica Serovar Typhi ◽  
Type Iv ◽  
Reference Collection ◽  
First Time

ABSTRACT Salmonella enterica serotype Typhi differs from nontyphoidal Salmonella serotypes by its strict host adaptation to humans and higher primates. Since fimbriae have been implicated in host adaptation, we investigated whether the serotype Typhi genome contains fimbrial operons which are unique to this pathogen or restricted to typhoidal Salmonella serotypes. This study established for the first time the total number of fimbrial operons present in an individual Salmonella serotype. The serotype Typhi CT18 genome, which has been sequenced by the Typhi Sequencing Group at the Sanger Centre, contained a type IV fimbrial operon, an orthologue of the agf operon, and 12 putative fimbrial operons of the chaperone-usher assembly class. In addition tosef, fim, saf, and tcf, which had been described previously in serotype Typhi, we identified eight new putative chaperone-usher-dependent fimbrial operons, which were termedbcf, sta, stb, ste, std, stc, stg, and sth. Hybridization analysis performed with 16 strains ofSalmonella reference collection C and 22 strains ofSalmonella reference collection B showed that all eight putative fimbrial operons of serotype Typhi were also present in a number of nontyphoidal Salmonella serotypes. Thus, a simple correlation between host range and the presence of a single fimbrial operon seems at present unlikely. However, the serotype Typhi genome differed from that of all other Salmonella serotypes investigated in that it contained a unique combination of putative fimbrial operons.

scholarly journals Multiple layers of heterogeneity and subset diversity in human MAIT cell responses to distinct microorganisms and to innate cytokines

2017 ◽  
Vol 114 (27) ◽  
pp. E5434-E5443 ◽  
Author(s):  
Joana Dias ◽  
Edwin Leeansyah ◽  
Johan K. Sandberg
Keyword(s):  
Killer Cell ◽  
Cell Subset ◽  
Effector Memory ◽  
Response Patterns ◽  
E Coli ◽  
Mait Cells ◽  
Cell Responses ◽  
Fungal Organisms ◽  
Subset Diversity ◽  
Mait Cell

Mucosa-associated invariant T (MAIT) cells are a large innate-like T-cell subset in humans defined by invariant TCR Vα7.2 use and expression of CD161. MAIT cells recognize microbial riboflavin metabolites of bacterial or fungal origin presented by the monomorphic MR1 molecule. The extraordinary level of evolutionary conservation of MR1 and the limited known diversity of riboflavin metabolite antigens have suggested that MAIT cells are relatively homogeneous and uniform in responses against diverse microbes carrying the riboflavin biosynthesis pathway. The ability of MAIT cells to exhibit microbe-specific functional specialization has not been thoroughly investigated. Here, we found that MAIT cell responses against Escherichia coli and Candida albicans displayed microbe-specific polyfunctional response profiles, antigen sensitivity, and response magnitudes. MAIT cell effector responses against E. coli and C. albicans displayed differential MR1 dependency and TCR β-chain bias, consistent with possible divergent antigen subspecificities between these bacterial and fungal organisms. Finally, although the MAIT cell immunoproteome was overall relatively homogenous and consistent with an effector memory-like profile, it still revealed diversity in a set of natural killer cell-associated receptors. Among these, CD56, CD84, and CD94 defined a subset with higher expression of the transcription factors promyelocytic leukemia zinc finger (PLZF), eomesodermin, and T-bet and enhanced capacity to respond to IL-12 and IL-18 stimulation. Thus, the conserved and innate-like MAIT cells harbor multiple layers of functional heterogeneity as they respond to bacterial or fungal organisms or innate cytokines and adapt their antimicrobial response patterns in a stimulus-specific manner.

scholarly journals Salmonella enterica Serovar Typhi Impairs CD4 T Cell Responses by Reducing Antigen Availability

2014 ◽  
Vol 82 (6) ◽  
pp. 2247-2254 ◽  
Author(s):  
S. M. Atif ◽  
S. E. Winter ◽  
M. G. Winter ◽  
S. J. McSorley ◽  
A. J. Baumler
Keyword(s):  
T Cell ◽  
Salmonella Enterica ◽  
T Cell Responses ◽  
Cd4 T Cell ◽  
Salmonella Enterica Serovar Typhi ◽  
Cell Responses

scholarly journals Linear plasmids and their replication

2013 ◽  
Vol 2 (1) ◽  
pp. 1-5 ◽  
Author(s):  
Sunjukta Ahsan ◽  
Md Shahidul Kabir
Keyword(s):  
Causative Agent ◽  
Salmonella Enterica ◽  
The Other ◽  
Linear Plasmid ◽  
Covalent Attachment ◽  
Common Belief ◽  
Replication Machinery ◽  
Linear Plasmids ◽  
Salmonella Enterica Serovar Typhi ◽  
First Time

It is still a common belief that plasmids are circular. However, linear plasmids have been reported to exist more than a decade ago. Two types of linear plasmids are known. One type contains covalently closed ends and are commonly found in Borrelia, the causative agent of tick fever. The other type is characterized by the covalent attachment of proteins at the 5' ends and exists in a number of bacterial genera including Streptomyces, Rhodococcus, Mycobacterium and Planobispora. Recently, a linear plasmid in Salmonella enterica serovar Typhi of the Enterobacteriaceae family have been reported for the first time. This paper reviews various postulated mechanisms of replication of linear plasmids and focuses on the components of the replication machinery of linear plasmids studied to date. DOI: http://dx.doi.org/10.3329/sjm.v2i1.15200 Stamford Journal of Microbiology, Vol.2(1) 2012: 1-5

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